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2,333,100 |
Linkage disequilibrium analyses of natriuretic peptide precursor B locus reveal risk haplotype conferring high plasma BNP levels.
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Brain natriuretic peptide (BNP) has been widely used for the diagnosis and prognostic evaluation of chronic heart failure (CHF). In the present study, we performed association study of single nucleotide polymorphisms (SNPs) surrounding the natriuretic peptide precursor B (NPPB) gene with plasma BNP levels in 2970 adult Japanese.</AbstractText>Association analysis between SNPs of the NPPB gene and plasma BNP revealed significant associations of the 8 SNPs surrounding the entire NPPB gene with plasma BNP levels. For instance, as to SNP rs198389 (T-381C), plasma BNP levels among the three genotypic categories, i.e., 2189 homozygous T-allele carriers (BNP 26.4+/-0.6pg/ml), 697 heterozygous carriers (35.0+/-1.1pg/ml), and 52 homozygous C-allele carriers (46.0+/-4.1pg/ml) indicated a co-dominant effect of the minor C-allele on elevating plasma BNP levels (P<0.0001). Linkage disequilibrium (LD) analysis among the 8 SNPs revealed that the region consisted of two, 5' major and 3' minor, LD blocks. Haplotype-based association analysis demonstrated that plasma BNP levels were associated closely with the haplotypes-1 and -2 of the major LD block.</AbstractText>These results suggest that genetic variation at the primary locus NPPB gene, represented by definition of risk haplotypes, may be an important determinant of plasma BNP levels.</AbstractText>
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2,333,101 |
Riluzole and D-amphetamine interactions in humans.
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In preclinical studies, medications which decrease glutamate release have been shown to block some of the effects of psychostimulants. One such medication is riluzole, marketed for the treatment of Amyotrophic Lateral Sclerosis (ALS). The goal of this study was to determine riluzole's effects on acute physiological and subjective responses to d-amphetamine in healthy volunteers. Seven male and 5 female subjects participated in an outpatient double-blind, placebo-controlled, crossover study. Across 4 sessions, subjects were randomly assigned to a sequence of 4 oral treatments: placebo, 20 mg D-amphetamine alone, 100 mg riluzole alone, or d-amphetamine plus riluzole. Outcome measures included heart rate, blood pressure, plasma cortisol, performance on the Sustained Attention to Response Test (SART), and subjective measures. d-amphetamine increased heart rate, blood pressure and plasma cortisol levels while inducing psychostimulant-type subjective effects. On the SART, d-amphetamine enhanced the speed of correct responses but also significantly increased the number of errors of commission. Riluzole at 100 mg did not block, the typical subjective and physiological responses to 20 mg D-amphetamine. Riluzole alone induced amphetamine-like subjective responses. On the SART test, riluzole increased the number errors of commission, but unlike d-amphetamine, did not speed reaction time. The mechanism accounting for these findings is unclear, but may involve processes other than decreased glutamate release by riluzole. The effects of glutamate medications on psychostimulant responses need to be further examined.
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2,333,102 |
Vasopressin dysregulation and hyponatremia in hospitalized patients.
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Hyponatremia, which is often due to dysregulation of arginine vasopressin, occurs frequently in hospitalized patients and is associated with increased morbidity and mortality. Nonosmotic secretion of arginine vasopressin is central to the pathophysiology of hyponatremia in patients with euvolemic hyponatremia (due to, for example, the syndrome of inappropriate secretion of antidiuretic hormone) and those with hypervolemic hyponatremia secondary to congestive heart failure or cirrhosis with ascites. Arginine vasopressin-receptor antagonists, a novel class of agents that block the action of arginine vasopressin on V2 receptors in the renal collecting ducts, may provide specific correction of sodium and water imbalance in hyponatremia by promoting free water clearance while sparing electrolytes (aquaresis). Arginine vasopressin antagonism would treat hyponatremia directly, as opposed to other therapies that do not address the effects of arginine vasopressin dysregulation directly.
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2,333,103 |
Effect of muscle relaxants on heart rate, arterial pressure, intubation conditions and onset of neuromuscular block in patients undergoing valve surgery.
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Sixty six patients undergoing elective valve surgery were randomized to receive rocuronium bromide 0.6 mg/Kg (Group R, n=22), pancuronium bromide 0.1 mg/Kg (Group P, n= 22) and vecuronium bromide 0.1 mg/Kg (Group V, n=22), Measurements of heart rate and arterial pressure (systolic, diastolic and mean) were noted at the following stages: 1) baseline when haemodynamics were stable for 2 minutes after induction of anaesthesia (2) one, (3) three, (4) five minutes after administration of muscle relaxants, (5) One, (6) three, and (7) five minutes after intubation. In group R, the heart rate decreased 5 min after injection of muscle relaxant from 93.9 +/- 21.3 to 82.4 +/- 20.7 beats/min (p<0.001). However, it increased to 128.3 +/- 25.8 beats/min (p<0.001) following intubation and returned to baseline at 5 min after intubation. In group P, heart rate increased from 98.8 +/- 32.6 to 109.6 +/- 32.7 beats/min (p<0.001), 1 min after injection of pancuronium and this increase persisted throughout the study period. In group V, heart rate decreased from 99.9 +/- 22.3 to 83.8 +/-19.6 beats/min (p<0.001) at 5 min after injection of the drug. It increased to 118.6 +/- 22.4 beats/min (p<0.001), 1 min after intubation and returned to baseline at 5 min after intubation. The decrease in heart rate in group R and V was accompanied by a significant decrease in systolic, diastolic and mean arterial pressure. In group P, only the systolic pressure decreased significantly at 5 min after injection of the drug. Intubation was accompanied by a significant increased in systolic, diastolic and mean arterial pressure in all the groups. Excellent intubation conditions (intubation score 3-4) were observed with all the three drugs, however, there were number of patients in group P who showed diaphragmatic movement during intubation. Onset of action of muscle relaxant, was fastest with rocuronium (group R=132.7 +/- 0.3 sec, P=182.6 +/- 68.5 sec, V= 144.8 +/- 46.1 sec, Group P vs Group R). To conclude, pancuronium causes significant increase in heart rate and should be preferred in patients with regurgitant lesions having slower baseline heart rate. Vecuronium and rocuronium decrease the heart rate and should be preferred in patient with faster baseline heart rate. In terms of intubating conditions rocuronium and vecuronium provide best conditions, but onset is faster with rocuronium.
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2,333,104 |
Selective genotyping reveals association between the epithelial sodium channel gamma-subunit and systolic blood pressure.
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Systolic blood pressure is determined in large part by genes. Six independent studies have reported evidence of linkage between systolic pressure and chromosome 16p12 that incorporates SCNN1G, the gene encoding the gamma-subunit of the epithelial sodium channel. We undertook the first comprehensive association analysis of SCNN1G and systolic pressure. To achieve genetic contrast, we sampled unrelated subjects within the upper (mean: 166 mm Hg; n=96) and lower (mean: 98 mm Hg; n=94) 10% of the systolic pressure distribution of 2911 subjects from the Victorian Family Heart Study. We examined genotypes and haplotypes related to 26 single nucleotide polymorphisms across SCNN1G and its promoter. Each of 3 single nucleotide polymorphisms (rs13331086, rs11074553, and rs4299163) in introns 5 and 6 showed evidence of association with systolic pressure in logistic regression analyses adjusted for age, sex, and body mass index. Considered as a haplotype block, these single nucleotide polymorphisms were significantly associated with systolic pressure (haplo.score global: P=0.0001). In permutation analyses to account for multiple testing, a result such as this was observed only once in 10,000 permutations. The estimated frequency of 1 haplotype (TGC) was substantially greater in high (13.3%) than low (0.6%) systolic pressure subjects (P=0.0001). Three other haplotypes (TGG, TAC, and GGC) showed associations with high or low systolic pressure consistent with the observed associations of their composite alleles. These findings identify relatively common polymorphisms in the SCNN1G gene that are associated with high systolic blood pressure in the general Australian white population.
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2,333,105 |
Central sympatholysis as a novel countermeasure for cocaine-induced sympathetic activation and vasoconstriction in humans.
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The aim of this study was to determine whether cocaine's sympathomimetic actions can be reversed by a potent centrally acting alpha2 adrenergic receptor (AR) agonist (dexmedetomidine).</AbstractText>We recently showed that cocaine stimulates the human cardiovascular system primarily by acting in the brain to increase sympathetic nerve activity (SNA), the neural stimulus to norepinephrine release. Thus, SNA constitutes a putative new drug target to block cocaine's adverse cardiovascular effects at their origin.</AbstractText>In 22 healthy cocaine-naïve humans, we measured skin SNA (microneurography) and skin blood flow (laser Doppler velocimetry) as well as heart rate and blood pressure before and after intranasal cocaine (2 mg/kg) alone and in combination with dexmedetomidine or saline.</AbstractText>During intranasal cocaine alone, SNA increased by 2-fold and skin vascular resistance increased from 13.2 +/- 2.3 to 20.1 +/- 2.2 resistance units while mean arterial pressure increased by 14 +/- 3 mm Hg and heart rate by 18 +/- 3 beats/min (p < 0.01). Dexmedetomidine abolished these increases, whereas intravenous saline was without effect. Dexmedetomidine was effective in blocking these sympathomimetic actions of cocaine even in all 7 subjects who were homozygous for the Del322-325 polymorphism in the alpha2C AR, a loss-of-function mutation that is highly enriched in blacks.</AbstractText>The data advance the novel hypothesis that central sympatholysis with dexmedetomidine constitutes a highly effective countermeasure for cocaine's sympathomimetic actions on the human cardiovascular system, even in individuals carrying the alpha2CDel322-325 polymorphism. (Study to Improve Scientific Understanding of the Cardiovascular Actions of Cocaine; http://clinicaltrials.gov/ct/show/NCT00338546?order=1; NCT00338546).</AbstractText>
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2,333,106 |
Nitric oxide donor isosorbide mononitrate for pre-induction cervical ripening at 41 weeks' gestation: A randomized controlled trial.
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Nitric oxide donors have been shown to cause cervical ripening. The aim of this study was to determine whether sustained release isosorbide mononitrate (ISMN-SR) 60 mg administered vaginally is effective for pre induction cervical ripening at 41 weeks' gestation.</AbstractText>A double-blind randomised controlled trial was carried out at the University Obstetric Unit, Galle, Sri Lanka for a period of 9 months, commencing 1st August 2003. One hundred and fifty-six consecutive women with uncomplicated singleton pregnancies at 41 weeks' gestation with a modified Bishop Score <5 were allocated by stratified (primip/multip) block randomization to receive either ISMN-SR 60 mg (n = 78) or vitamin C 100 mg (n = 78) vaginally. Modified Bishop Score at 41 weeks + 2 days' gestation and the proportions establishing spontaneous labor or becoming favorable for induction of labor (IOL) by 41 weeks + 2 days' gestation were evaluated in each group.</AbstractText>At the commencement of the study there were no differences between the mean age, parity or modified Bishop Score of the two groups. In the ISMN-SR group, there was a marked increase in the proportion establishing spontaneous labor (28% vs 7.5%, P < 0.01) and being favorable for IOL (40% vs 9% P < 0.001), 2 days after therapy. In the ISMN-SR group, there was a significantly higher increase in the mean modified Bishop Score (3.8, 95% CI 2.3-5.3 vs 1.3, 95% CI 0.3-2.2, P < 0.01) and a marked decrease in the proportion of subjects requiring further ripening of the cervix with a Foley catheter. (32% vs 79%, P < 0.001). The cesarean section rates were similar in both groups.</AbstractText>Sustained release ISMN administered vaginally is effective for preinduction cervical ripening.</AbstractText>
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2,333,107 |
Spinal anesthesia for endoscopic urological surgery--low dose vs. varying doses of hyperbaric bupivacaine.
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The aim of this study is to compare the efficiency of low dose vs. varying doses of hyperbaric bupivacaine in spinal anesthesia for endoscopic urological procedures.</AbstractText>Sixty consecutive patients were studied in a randomized prospective manner. They received either of 5 (Gr I), 7.5 (Gr II) or 10 mg (Gr III) of hyperbaric bupivacaine 0.5% combined with 25 microg of fentanyl, through a 25-gauge W hitacre spinal needle placed in the L3-L4 interspace. Characteristics of sensory and motor block, dose of ephedrine required, secondary effects, the patients, and the surgeons satisfaction, were noted.</AbstractText>The maximum number of blocked segments was 14 +/- 1 (Gr I), 15 +/- 2 (Gr II) and 16 +/- 2 (Gr III). Time to T12 regression was significantly shorter for Gr I (53 +/- 13 min) than for Gr II (69 +/- 20 min) or Gr III (94 +/- 14 min). Bromage 3 block was not found in Gr I compared to 4 patients in Gr II and 15 patients in Gr III. The duration of motor block was shorter in Gr 1(51 +/- 18 min) than in Gr II (86 +/- 19 min) and in Gr III (138 +/- 21 min). Ephedrine was used for 16 patients in Gr III (9.8 +/- 12.2 mg), 5 patients in Gr II (3.7 +/- 7.8 mg) and 2 patients in Gr I (0.5 +/- 1.5 mg). The difference is statistically significant between Gr III and the other groups.</AbstractText>These results suggest that the use of a low dose of bupivacaine (5 mg) added to fentanyl (25 microg) for endoscopic urological surgery, resulted in short-acting sensory block, without motor block and a lower incidence of cardiovascular side effects, as compared to either of 7.5 or 10 mg bupivacaine with 25 microg fentanyl.</AbstractText>
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2,333,108 |
A role for heme oxygenase-1 in the immunosuppressive effect of adult rat and human mesenchymal stem cells.
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Mesenchymal stem cells (MSCs) display immunomodulatory properties mediated by various factors, including inducible nitric oxide synthase (iNOS). Since heme oxygenase-1 (HO-1) is a potent immunosuppressive enzyme, we tested the hypothesis that HO-1 could mediate the immunosuppressive effects of MSCs. We generated adult rat MSCs that inhibited T-cell proliferation in vitro. These MSCs expressed both HO-1 and iNOS. In vitro, whereas neither HO-1 nor iNOS inhibition alone could interfere with the immunosuppressive properties of rat MSCs, simultaneous inhibition of both enzymes restored T-cell proliferation. In vivo, injection of MSCs significantly delayed heart allograft rejection, and inhibition of either HO-1 or iNOS totally reversed the protective activity of MSCs, inducing rejection. Adult human MSCs also expressed HO-1; in these cells, HO-1 inhibition was sufficient to completely block their immunosuppressive capacity. In conclusion, we show, for the first time, that HO-1 mediates the immunosuppressive properties of rat and human MSCs.
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2,333,109 |
Analgesic efficacy of bilateral superficial cervical plexus block administered before thyroid surgery under general anaesthesia.
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The use of regional anaesthesia in thyroid surgery remains controversial. This double-blind, randomized controlled study was conducted to evaluate the analgesic efficacy of bilateral superficial cervical plexus block (BSCPB) performed under general anaesthesia in patients undergoing total thyroidectomy.</AbstractText>Eighty-seven consecutive consenting patients were randomized to receive a BSCPB with saline (Group P, n = 29), ropivacaine 0.487% (Group R, n = 29), or ropivacaine 0.487% plus clonidine 5 microg ml(-1) (Group RC, n = 29). Sufentanil was given during the intraoperative period for a 20% increase in arterial mean pressure or heart rate in a patient with a bispectral index between 40 and 60. All patients received 4 g of acetaminophen during the first 24 h after operation. The pain score was checked every 4 h and nefopam was given for pain score >4 on a numeric pain scale.</AbstractText>During surgery, the median sufentanil requirements were significantly reduced in Group RC compared with Groups R and P (0.32 vs 0.47 and 0.62 microg kg(-1); P < 0.0001). After surgery, the number of patients requiring nefopam within 24 h of surgery was significantly lower in Groups R and RC than in Group P (16 and 19 vs 25; P = 0.03). At post-anaesthetic care unit admission, median (range) pain scores were significantly lower in Groups R [3 (0-10)] and RC [3 (0-8)] than in Group P [5 (0-8), P = 0.03]. No major complications of BSCPB occurred during study.</AbstractText>BSCPB with ropivacaine and clonidine improved intraoperative analgesia. BSCPB with ropivacaine or ropivaciane and clonidine was effective in reducing analgesic requirements after thyroid surgery.</AbstractText>
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2,333,110 |
A computational approach to predict pulse transit time variations during postural change.
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The human autonomic nervous system modulates blood pressure (BP) and heart rate in order to maintain homeostasis. Present techniques that monitor BP may cause discomforts to children. Pulse transit time change (DeltaPTT) is known to be inversely correlated to BP change. In this study, a mathematical model using only a few empirical parameters and the measured lower limb vascular path length is introduced to estimate DeltaPTT when a different posture is adopted. To assess the reliability of the model, 23 healthy children aged 8.4 +/- 2.3 years were recruited to adopt the sitting and supine position at discrete intervals. PTT measurements were obtained from their toe with respect to an ECG for both postures. The results showed that there was significant correlation between the model and measured DeltaPTT (P < 0.05; R(2) = 0.813). The findings herein suggest that this simple yet practical model can have the accuracy to estimate the DeltaPTT value. Moreover, it does not require the use of an ECG or pulse oximeter in its computation. Hence, it can provide a rapid prediction before a child adopts a postural change. This may be potentially useful for detection of children with vascular abnormalities at their lower limbs.
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2,333,111 |
An update on the management of Chagas cardiomyopathy.
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Chagas disease, caused by the protozoan parasite Trypanosoma cruzi, infects nearly 18 million people in Latin America and mainly affects the heart, causing heart failure, arrhythmias, heart block, thromboembolism, stroke and death. In this review, the clinical diagnosis and management of Chagas cardiomyopathy are discussed. Particular emphasis is placed on the clinical staging of patients and the use of various diagnostic tests that may be useful in individualizing treatment of the two most relevant clinical syndromes, that is, heart failure and arrhythmias. The relevance of specific treatments are discussed, stressing the important role of parasite persistence in disease pathogenesis. We also discuss new therapy modalities that may have a role in the treatment of Chagas cardiomyopathy.
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2,333,112 |
Comparison of midazolam, propofol and fentanyl combinations for sedation and hemodynamic parameters in cataract extraction.
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Midazolam, propofol and fentanyl were compared in terms of sedation during cataract extraction. Hemodynamic parameters, sedation level, postoperative satisfaction, and side effects were investigated.</AbstractText>The study was carried out in Hacettepe University Hospitals Ophthalmology Operating Theatres in 2005. The patients received only midazolam (0.02 mg kg-1), or midazolam (0.02 mg kg-1) + propofol (0.2 mg kg-1), or midazolam (0.02 mg kg-1) + fentanyl (1 microgram kg-1), or midazolam (0.02 mg kg-1) + propofol (0.2 mg kg-1) + fentanyl (1 microgram kg-1). The sedation level of patients was measured according to a physician questionnaire. Postoperative nausea/vomiting, headache, and patient satisfaction were determined via a patient's evaluation scale.</AbstractText>In the groups receiving fentanyl, the hemodynamic response to peribulbar block insertion was minimal (p<0.05) and the sedation level was best (p<0.05). Respiration rate and O2 saturation of patients receiving midazolam, propofol, and fentanyl decreased after sedation (p<0.01) and postoperative satisfaction was high in this group (p<0.01). Patients in the midazolam group showed a prominent reaction to peribulbar block insertion while movement during the operation was obvious (p<0.05).</AbstractText>The combination of midazolam, propofol, and fentanyl should be preferred to other study groups as the sedation level is suitable for cataract extraction with high postoperative patient satisfaction and without any side effects.</AbstractText>
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2,333,113 |
Metabolic forearm vasodilation is enhanced following Bier block with phentolamine.
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The extent to which sympathetic nerve activity restrains metabolic vasodilation in skeletal muscle remains unclear. We determined forearm blood flow (FBF; ultrasound/Doppler) and vascular conductance (FVC) responses to 10 min of ischemia [reactive hyperemic blood flow (RHBF)] and 10 min of systemic hypoxia (inspired O(2) fraction = 0.1) before and after regional sympathetic blockade with the alpha-receptor antagonist phentolamine via Bier block in healthy humans. In a control group, we performed sham Bier block with saline. Consistent with alpha- receptor inhibition, post-phentolamine, basal FVC (FBF/mean arterial pressure) increased (pre vs. post: 0.42 +/- 0.05 vs. 1.03 +/- 0.21 units; P < 0.01; n = 12) but did not change in the saline controls (pre vs. post: 0.56 +/- 0.14 vs. 0.53 +/- 0.08 units; P = not significant; n = 5). Post-phentolamine, total RHBF (over 3 min) increased substantially (pre vs. post: 628 +/- 75 vs. 826 +/- 92 ml/min; P < 0.01) but did not change in the controls (pre vs. post: 618 +/- 66 vs. 661 +/- 35 ml/min; P = not significant). In all conditions, compared with peak RHBF, peak skin reactive hyperemia was markedly delayed. Furthermore, post-phentolamine (pre vs. post: 0.43 +/- 0.06 vs. 1.16 +/- 0.17 units; P < 0.01; n = 8) but not post-saline (pre vs. post: 0.93 +/- 0.16 vs. 0.87 +/- 0.19 ml/min; P = not significant; n = 5), the FVC response to hypoxia (arterial O(2) saturation = 77 +/- 1%) was markedly enhanced. These data suggest that sympathetic vasoconstrictor nerve activity markedly restrains skeletal muscle vasodilation induced by local (forearm ischemia) and systemic (hypoxia) vasodilator stimuli.
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2,333,114 |
Vasopressin-receptor antagonist therapy in patients with hyponatraemia.
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Hyponatraemia often complicates the treatment of underlying conditions in patients who are seriously ill. Arginine vasopressin receptor antagonists block the action of arginine vasopressin and correct sodium and water imbalance in patients with euvolaemic or hypervolaemic hyponatraemia.
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2,333,115 |
Oestrogen directly inhibits the cardiovascular L-type Ca2+ channel Cav1.2.
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Oestrogen can modify the contractile function of vascular smooth muscle and cardiomyocytes. The negative inotropic actions of oestrogen on the heart and coronary vasculature appear to be mediated by L-type Ca(2+) channel (Ca(v)1.2) inhibition, but the underlying mechanisms remain elusive. We tested the hypothesis that oestrogen directly inhibits the cardiovascular L-type Ca(2+) current, I(CaL). The effect of oestrogen on I(CaL) was measured in Ca(v)1.2-transfected HEK-293 cells using the whole-cell patch-clamp technique. The current revealed typical activation and inactivation profiles of nifedipine- and cadmium-sensitive I(CaL). Oestrogen (50 microM) rapidly reduced I(CaL) by 50% and shifted voltage-dependent activation and availability to more negative potentials. Furthermore, oestrogen blocked the Ca(2+) channel in a rate-dependent way, exhibiting higher efficiency of block at higher stimulation frequencies. Our data suggest that oestrogen inhibits I(CaL) through direct interaction of the steroid with the channel protein.
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2,333,116 |
The Na+/Ca2+ exchange inhibitor KB-R7943 potently blocks TRPC channels.
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Na(+)/Ca(2+) exchangers (NCXs) and members of the canonical transient receptor potential (TRPC) channels play an important role in Ca(2+) homeostasis in heart and brain. With respect to their overlapping expression and their role as physiological Ca(2+) influx pathways a functional discrimination of both mechanisms seems to be necessary. Here, the effect of the reverse-mode NCX inhibitor KB-R7943 was investigated on different TRPC channels heterologously expressed in HEK293 cells. In patch-clamp recordings KB-R7943 potently blocked currents through TRPC3 (IC(50)=0.46 microM), TRPC6 (IC(50)=0.71 microM), and TRPC5 (IC(50)=1.38 microM). 1-Oleoyl-2-acetyl-sn-glycerol-induced Ca(2+) entry was nearly completely suppressed by 10 microM KB-R7943 in TRPC6-transfected cells. Thus, KB-R7943 is able to block receptor-operated TRP channels at concentrations which are equal or below those required to inhibit reverse-mode NCX activity. These data further suggest that the protective effects of KB-R7943 in ischemic tissue may, at least partly, be due to inhibition of TRPC channels.
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2,333,117 |
Cardiovascular influence of dental anxiety during local anesthesia for tooth extraction.
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The present study evaluated whether dental patient anxiety has an effect on the cardiovascular response to the delivery of anesthetic to achieve mandibular anesthesia.</AbstractText>One hundred eighty adult patients scheduled to receive routine dental extraction under local anesthesia were enrolled in this prospective study. Anxiety was measured at 15 minutes before local anesthetic delivery using Corah's Dental Anxiety Scale (Corah's DAS). Anesthetic was delivered using a standard technique for mandibular nerve block with the same dose (2 cartridges) given to all patients. Cardiovascular response data including blood pressure, heart rate, O(2) saturation, and electrocardiographic changes were measured at 5 time points from 5 minutes before to 15 minutes after the administration of anesthetic.</AbstractText>The mean anxiety scale score before administration of anesthetic was 9.3 (SD +/- 2.5) with a range from 4 to 20. Women had a significantly higher mean dental anxiety level than men (P < .05). Younger age was associated with a higher anxiety scale score. Severe preoperative anxiety (Corah's DAS >12) was associated with significantly increased heart rate during administration of anesthetic. Patients with severe anxiety also had a significantly greater increase in heart rate during anesthetic administration (P < .001). Younger age was associated with increased likelihood of high dental anxiety and associated cardiovascular response to dental anesthesia (P = .001). Pain on injection was also associated with increased heart rate during anesthetic administration.</AbstractText>This study showed that Corah's dental anxiety scale is a useful tool for estimating the impact of anxiety on the heart rate during local anesthetic delivery to achieve mandibular block for dental extraction. Younger patients undergoing tooth extraction were more likely to have high anxiety levels, and younger patients with high anxiety were more likely to report a traumatic dental history. High anxiety, younger age, and traumatic dental history were correlated with greater increases in heart rate during the administration of local dental anesthesia.</AbstractText>
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2,333,118 |
Aldosterone induces circadian gene expression of clock genes in H9c2 cardiomyoblasts.
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We examined mRNA expression of the clock genes (Per1, Per2, and Bmal1) and PAI-1 (plasminogen activator inhibitor-1) after aldosterone treatment every 4 h up to 48 h in H9c2 cardiomyoblasts by reverse transcription-polymerase chain reaction. To block the MR (mineralocorticoid receptor), the MR antagonist, spironolactone, was added to the medium 1 h before aldosterone treatment. Aldosterone induced an initial increase and rhythmic expression of Per1, while spironolactone attenuated the acute increase in Per1 mRNA induced by aldosterone. On the other hand, aldosterone did not increase the Per2 mRNA in the acute phase, but thereafter induced a rhythmic expression of Per2. Aldosterone also induced rhythmic expression of Bmal1, a positive element of the clock genes. The rhythm of Bmal1 mRNA was anti-phase of that of Per2 mRNA. Aldosterone induced an acute increase in PAI-1 mRNA, but did not induce rhythmic expression of PAI-1. The present study demonstrated first that aldosterone regulates expression of the clock genes Per1, Per2, and Bmal1, and increases PAI-1 expression in H9c2 cardiomyoblasts. Second, an acute increase in Per1 mRNA after aldosterone treatment is mediated through MR. Third, clock genes are not related to PAI-1 expression in H9c2 cardiomyoblasts.
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2,333,119 |
Neurological outcome in isolated congenital heart block and hydrops fetalis.
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Isolated fetal heart block (HB), a condition associated with fetal hydrops, carries a high mortality rate and may result in neurodevelopmental sequelae. To the best of our knowledge, no data exist regarding the long-term outcome of such hydropic fetuses. We reviewed our experience with this condition to determine the neurodevelopmental outcome of prenatally diagnosed cases with isolated HB complicated by hydrops fetalis.</AbstractText>Neurodevelopmental assessment of 5 children presented prenatally with isolated HB associated with hydrops fetalis.</AbstractText>During the last 18 years, 10 cases were detected prenatally with isolated HB and hydrops fetalis. 3 of the 10 fetuses died in utero, and 2 died postnatally, due to a dilated cardiomyopathy, at the age of 9 months and 4 years, respectively. Neurodevelopmental studies done on the 5 remaining children were normal.</AbstractText>Long-term neurodevelopmental assessments of 5 surviving cases presented prenatally with isolated HB and hydrops fetalis are reassuring.</AbstractText>Copyright 2007 S. Karger AG, Basel.</CopyrightInformation>
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2,333,120 |
Xenografted adult human mesenchymal stem cells provide a platform for sustained biological pacemaker function in canine heart.
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Biological pacemaking has been performed with viral vectors, human embryonic stem cells, and adult human mesenchymal stem cells (hMSCs) as delivery systems. Only with human embryonic stem cells are data available regarding stability for >2 to 3 weeks, and here, immunosuppression has been used to facilitate survival of xenografts. The purpose of the present study was to determine whether hMSCs provide stable impulse initiation over 6 weeks without the use of immunosuppression, the "dose" of hMSCs that ensures function over this period, and the catecholamine responsiveness of hMSC-packaged pacemakers.</AbstractText>A full-length mHCN2 cDNA subcloned in a pIRES2-EGFP vector was electroporated into hMSCs. Transfection efficiency was estimated by GFP expression. I(HCN2) was measured with patch clamp, and cells were administered into the left ventricular anterior wall of adult dogs in complete heart block and with backup electronic pacemakers. Studies encompassed 6 weeks. I(HCN2) for all cells was 32.1+/-1.3 pA/pF (mean+/-SE) at -150 mV. Pacemaker function in intact dogs required 10 to 12 days to fully stabilize and persisted consistently through day 42 in dogs receiving > or =700,000 hMSCs (approximately 40% of which carried current). Rhythms were catecholamine responsive. Tissues from animals killed at 42 days manifested neither apoptosis nor humoral or cellular rejection.</AbstractText>hMSCs provide a means for administering catecholamine-responsive biological pacemakers that function stably for 6 weeks and manifest no cellular or humoral rejection at that time. Cell doses >700,000 are sufficient for pacemaking when administered to left ventricular myocardium.</AbstractText>
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2,333,121 |
Effects of Chinese herbs on multiple ion channels in isolated ventricular myocytes.
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Shensong Yangxin (SSYX) is one of the compound recipe of Chinese materia medica. This study was conducted to investigate the effects of SSYX on sodium current (I(Na)), L-type calcium current (I(Ca, L)), transient outward potassium current (I(to)), delayed rectifier current (I(K)), and inward rectifier potassium currents (I(K1)) in isolated ventricular myocytes.</AbstractText>Whole cell patch-clamp technique was used to study ion channel currents in enzymatically isolated guinea pig or rat ventricular myocytes.</AbstractText>SSYX decreased peak I(Na) by (44.84 +/- 7.65)% from 27.21 +/- 5.35 to 14.88 +/- 2.75 pA/pF (n = 5, P < 0.05). The medicine significantly inhibited the I(Ca, L). At concentrations of 0.25, 0.50, and 1.00 g/100 ml, the peak I(Ca, L) was reduced by (19.22 +/- 1.10)%, (44.82 +/- 6.50)% and (50.69 +/- 5.64)%, respectively (n = 5, all P < 0.05). SSYX lifted the I - V curve of both I(Na) and I(Ca, L) without changing the threshold, peak and reversal potentials. At the concentration of 0.5%, the drug blocked the transient component of I(to) by 50.60% at membrane voltage of 60 mV and negatively shifted the inactive curve and delayed the recovery from channel inactivation. The tail current density of I(K) was decreased by (30.77 +/- 1.11)% (n = 5, P < 0.05) at membrane voltage of 50 mV after exposure to the medicine and the time-dependent activity of I(K) was also inhibited. Similar to the effect on I(K), the SSYX inhibited I(K1) by 33.10% at the test potential of -100 mV with little effect on reversal potential and the rectification property.</AbstractText>The experiments revealed that SSYX could block multiple ion channels such as I(Na) I(Ca, L), I(k), I(to) and I(K1), which may change the action potential duration and contribute to some of its antiarrhythmic effects.</AbstractText>
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2,333,122 |
Pinto bean consumption reduces biomarkers for heart disease risk.
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To determine effects of daily intake of 1/2 cup pinto beans, black-eyed peas or carrots (placebo) on risk factors for coronary heart disease (CHD) and diabetes mellitus (DM) in free-living, mildly insulin resistant adults over an 8 week period.</AbstractText>Randomized, crossover 3x3 block design. Sixteen participants (7 men, 9 women) received each treatment for eight-weeks with two-week washouts. Fasting blood samples collected at beginning and end of periods were analyzed for total cholesterol (TC), low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol, triacylglycerols, high-sensitivity C-reactive protein, insulin, glucose, and hemoglobin A1c.</AbstractText>A significant treatment-by-time effect impacted serum TC (p = 0.026) and LDL (p = 0.033) after eight weeks. Paired t-tests indicated that pinto beans were responsible for this effect (p = 0.003; p = 0.008). Mean change of serum TC for pinto bean, black-eyed pea and placebo were -19 +/- 5, 2.5 +/- 6, and 1 +/- 5 mg/dL, respectively (p = 0.011). Mean change of serum LDL-C for pinto bean, black-eyed pea and placebo were -14 +/- 4, 4 +/- 5, and 1 +/- 4 mg/dL, in that order (p = 0.013). Pinto beans differed significantly from placebo (p = 0.021). No significant differences were seen with other blood concentrations across the 3 treatment periods.</AbstractText>Pinto bean intake should be encouraged to lower serum TC and LDL-C, thereby reducing risk for CHD.</AbstractText>
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2,333,123 |
The role of p53 in nitric oxide-induced cardiomyocyte cell death.
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The role of p53 in mediating nitric oxide (NO)-induced cell death remains uncertain. The exogenous NO donor S-nitrosoglutathione (GSNO) produced a concentration-dependent reduction in cell viability in embryonic chick cardiomyocytes in culture. Western blotting and immunocytochemistry for p53 showed that p53 was increased in whole cell lysates by GSNO: 0.001 mM GSNO led to 1.3 +/- 0.5-fold increase compared to control, and significantly (p < 0.05) increased to 1.6 +/- 0.2-fold after 0.01 mM GSNO. Higher GSNO concentrations did not further increase p53 protein expression despite producing significant increases in cell death. The p53 inhibitor pifithrin did not block GSNO-induced cell death. GSNO induced morphological changes of DNA fragmentation, nuclear condensation, and cell shrinkage. Pifithrin failed to block these morphologic changes, while it antagonized the similar cellular changes induced by adriamycin, which operates in part through p53. NO induced a concentration-dependent DNA damage. When assessed by the comet assay, the damage was 2.1 +/- 0.3-fold and 2.6 +/- 0.5-fold more than the control following 0.01 mM and 1.0 mM GSNO treatments, respectively. The DNA damage was not reduced by treatment with the pifithrin, which markedly reduced DNA damage induced by adriamycin. There was no p53 translocation to mitochondria, any major cytochrome c release from mitochondria, or change in mitochondrial membrane potential. Furthermore, cyclosporin A, which inhibits mitochondrial pore opening and cytochrome c loss, did not alter NO-induced cell death. Translocation of p53 from the cytosol to the nucleus occurred with a maximal increase of 2.9-fold in the nucleus following 1.0 mM GSNO for 24 h. These data indicate that in cardiomyocytes, NO induced marked DNA damage and translocation of p53 to the nucleus, suggesting that p53 is involved in the cellular response to NO, perhaps to modulate the genomic response to NO-induced cellular toxicity. NO-induced cell death, however, operates through p53-independent pathways, including a mitochondrial apoptotic pathway.
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2,333,124 |
Phosphatidylinositol 4,5-bisphosphate interactions with the HERG K(+) channel.
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Regulation of ion channel activity plays a central role in controlling heart rate, rhythm, and contractility responses to cardiovascular demands. Dynamic beat-to-beat regulation of ion channels is precisely adjusted by autonomic stimulation of cardiac G protein-coupled receptors. The rapidly activating delayed rectifier K(+) current (I (Kr)) is produced by the channel that is encoded by human ether-a-gogo-related gene (HERG) and is essential for the proper repolarization of the cardiac myocyte at the end of each action potential. Reduction of I (Kr) via HERG mutations or drug block can lead to lethal cardiac tachyarrhythmias. Autonomic regulation of HERG channels is an area of active investigation with the emerging picture of a complex interplay of signal transduction events, including kinases, second messengers, and protein-protein interactions. A recently described pathway for regulation of HERG is through channel interaction with the phospholipid phosphatidylinositol 4,5-bisphosphate (PIP2). Changes in cellular PIP2 concentrations may occur with Gq-coupled receptor activation. Here, we review the evidence for PIP2-HERG interactions, its potential biological significance, and unfilled gaps in our understanding of this regulatory mechanism.
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2,333,125 |
The clinical application of metabolic therapy for cardiovascular disease.
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Metabolic therapy involves the administration of a substance normally found in the body to enhance a metabolic reaction within the cell. This may be achieved in two ways. Firstly, for some systems a substance can be given to achieve greater than normal levels in the body so as to drive an enzymic reaction in a preferred direction. Secondly, metabolic therapy may be used to correct an absolute or relative deficiency of a cellular component. Thus, metabolic therapy differs greatly from most standard cardiovascular pharmacologic therapies such as the use of ACE Inhibitors, beta-blockers, statins and calcium channel antagonists that are given to block rather than enhance cellular processes.
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2,333,126 |
Association of P-wave duration, dispersion, and terminal force in relation to P-wave axis among outpatients.
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While P-wave duration (P-dur) and dispersion (P-disp) could both reflect fractionated and inhomogeneous propagation of sinus cardiac impulses, and may therefore be associated with each other, a clear relationship has not been extensively studied. We studied these markers as well as the significance of P-wave terminal force in lead V1 (PTFV1) in relation to the P-wave axis (P-axis).</AbstractText>We appraised our previously studied sample of 500 consecutively numbered, otherwise unselected, electrocardiograms (ECGs) of outpatients from the University of Massachusetts, Worcester, Massachusetts, for the foregoing P-wave characteristics. P-disp, defined as the difference of the duration between the widest and narrowest P wave, and the greatest P-dur after a 12-lead ECG search, was measured manually to the nearest 10 ms. PTFV1 was considered positive when > or = 40 mm2 terminal deflection was present on biphasic P waves on lead V1. Normal P-axis was considered 0 degrees to +75 degrees by manually constructing the mean frontal plane electrical P-axis from standard limb leads.</AbstractText>After excluding those with atrial arrhythmias, paced rhythms, errors in lead placement, P waves with low amplitude or overall technically poor tracing, 428 ECGs formed our final sample. P-dur was strongly associated with P-disp (P < 0.0001), but the correlation remained weak (r = 0.42). Overall, P-dur was not significantly associated with P-axis but when divided into tertiles and quintiles, the significance was evident within the range of the normal P-axis, particularly 0 degrees to +60 degrees (P < 0.0001). In a subanalysis of 380 ECGs that had appreciable biphasic P waves on lead V1, PTFV1 was noted on 178 (47%) ECGs and was significantly associated with P-dur (P < 0.0001), P-disp (P < 0.0001), and P-axis (P = 002). When considering P-axis in tertiles and quintiles, P-dur was greater in patients with a positive PTFV1 and significant within the normal range of the P-axis, especially from 0 degrees to +60 degrees .</AbstractText>P-dur, P-disp, and PTFV1 appear to share a significant tripartite association in relation to the normal P-axis, particularly when P-axis ranges 0 degrees to +60 degrees . Therefore, for optimal clinical assessment, these markers should be evaluated in relation to the normal P-axis.</AbstractText>
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2,333,127 |
Tumor necrosis factor-alpha in mechanic trauma plasma mediates cardiomyocyte apoptosis.
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Mechanical traumatic injury causes cardiomyocyte apoptosis and cardiac dysfunction. However, the signaling mechanisms leading to posttraumatic cardiomyocyte apoptosis remains unclear. The present study attempted to identify the molecular mechanisms responsible for cardiomyocyte apoptosis induced by trauma. Normal cardiomyocytes (NC) or traumatic cardiomyocytes (TC; isolated immediately after trauma) were cultured with normal plasma (NP) or traumatic plasma (TP; isolated 1.5 h after trauma) for 12 h, and apoptosis was determined by caspase-3 activation. Exposure of TC to NP failed to induce significant cardiomyocyte apoptosis. In contrast, exposure of NC to TP resulted in a greater than twofold increase in caspase-3 activation (P < 0.01). Incubation of cardiomyocytes with cytomix (a mixture of TNF-alpha, IL-1beta, and IFN-gamma) or TNF-alpha alone, but not with IL-1beta or IFN-gamma alone, caused significant caspase-3 activation (P < 0.01). TP-induced caspase-3 activation was virtually abolished by an anti-TNF-alpha antibody, and TP isolated from TNF-alpha(-/-) mice failed to induce caspase-3 activation. Moreover, incubation of cardiomyocytes with TP upregulated inducible nitric oxide (NO) synthase (iNOS)/NADPH oxidase expression, increased NO/superoxide production, and increased cardiomyocyte protein nitration (measured by nitrotyrosine content). These oxidative/nitrative stresses and the resultant cardiomyocyte caspase-3 activation can be blocked by neutralization of TNF-alpha (anti-TNF-alpha antibody), inhibition of iNOS (1400W), or NADPH oxidase (apocynin) and scavenging of peroxynitrite (FP15) (P < 0.01). Taken together, our study demonstrated that there exists a TNF-alpha-initiated, cardiomyocyte iNOS/NADPH oxidase-dependent, peroxynitrite-mediated signaling pathway that contributes to posttraumatic myocardial apoptosis. Therapeutic interventions that block this signaling cascade may attenuate posttraumatic cardiac injury and reduce the incidence of secondary organ dysfunction after trauma.
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2,333,128 |
[Urgent analgesia in a trauma patient].
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An 84-year-old patient with a fracture of the humerus suffered from severe pain. Analgesia was not sufficient using opioids. Because of a chronic heart disease a blockade of the brachial plexus was used for analgesia without any technical examination. The necessity of different medical examinations before block performance will be discussed.
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2,333,129 |
The role of the cyclooxygenase products in evoking sympathetic activation in exercise.
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Animal studies suggest that prostaglandins in skeletal muscles stimulate afferents and contribute to the exercise pressor reflex. However, human data regarding a role for prostaglandins in this reflex are varied, in part because of systemic effects of pharmacological agents used to block prostaglandin synthesis. We hypothesized that local blockade of prostaglandin synthesis in exercising muscles could attenuate muscle sympathetic nerve activity (MSNA) responses to fatiguing exercise. Blood pressure (Finapres), heart rate, and MSNA (microneurography) were assessed in 12 young healthy subjects during static handgrip and postexercise muscle ischemia (PEMI) before and after local infusion of 6 mg of ketorolac tromethamine in saline via Bier block (regional intravenous anesthesia). In the second experiment (n = 10), the same amount of saline was infused via the Bier block. Ketorolac Bier block decreased the prostaglandins synthesis to approximately 33% of the baseline. After ketorolac Bier block, the increases in MSNA from the baseline during the fatiguing handgrip was significantly lower than that before the Bier block (before ketorolac: Delta502 +/- 111; post ketorolac: Delta348 +/- 62%, P = 0.016). Moreover, the increase in total MSNA during PEMI after ketorolac was significantly lower than that before the Bier block (P = 0.014). Saline Bier block had no similar effect. The observations indicate that blockade of prostaglandin synthesis attenuates MSNA responses seen during fatiguing handgrip and suggest that prostaglandins contribute to the exercise pressor reflex.
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2,333,130 |
Small dose spinal bupivacaine for Cesarean delivery does not reduce hypotension but accelerates motor recovery.
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Maternal hypotension occurs in 60-94% of Cesarean deliveries with 10-15 mg spinal bupivacaine. Reduced doses of bupivacaine may decrease the incidence of hypotension, nausea, and vasopressor use. The primary objective of this study was to compare 4.5 mg and 12 mg doses of intrathecal bupivacaine on maternal hemodynamics. The secondary objective was to determine if anticipated reductions in side effects were reflected in increased patient satisfaction.</AbstractText>Following Research Ethics Board approval and informed consent 52 term parturients undergoing elective Cesarean delivery were randomly assigned to isobaric bupivacaine 4.5 mg or hyperbaric bupivacaine 12 mg for spinal anesthesia. All patients received fentanyl 50 microg and morphine 200 microg intrathecally. Intravenous fluid and vasopressor administration were standardized. Maternal hemodynamics, and sensorimotor levels were recorded at regular intervals. Side effects and patient satisfaction were documented.</AbstractText>Median cepahalad sensory block was C8 in both groups (NS) but the intensity of motor block was significantly less (P < 0.001) and of shorter duration (P < 0.001) with bupivacaine 4.5 mg. The proportion of patients requiring ephedrine (> 70%) and the quantities of ephedrine used were similar in both groups (NS). Use of supplemental analgesia, side effects, and measures of patient satisfaction were comparable in both groups.</AbstractText>Intrathecal bupivacaine 4.5 and 12 mg yielded similar sensory block and side effects during Cesarean delivery. Patients receiving 4.5 mg did, however, experience significantly less motor blockade of shorter duration.</AbstractText>
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2,333,131 |
Phosphodiesterase 4 inhibitors, rolipram and diazepam block the adaptive changes observed during morphine withdrawal in the heart.<Pagination><StartPage>1</StartPage><EndPage>9</EndPage><MedlinePgn>1-9</MedlinePgn></Pagination><Abstract><AbstractText>In this study, we investigated whether morphine dependence was inhibited by phosphodiesterase (PDE) 4 inhibitors rolipram and diazepam, since a role for the cyclic AMP systems in the development of morphine dependence was reported. Dependence of morphine was induced by a 7-day s.c. implantation of morphine pellets. Morphine withdrawal was precipitated on day 8 by an injection of naloxone. In order to determine the effect of rolipram or diazepam the animals were injected with these drugs for seven days and 30 min before the administration of naloxone. When opioid withdrawal was precipitated, enhancement of noradrenaline (NA) turnover in the heart was observed 30 min after naloxone administration. Moreover, morphine withdrawal induces Fos expression, increase in cyclic AMP and cyclic GMP levels. Co-administration of rolipram or diazepam with morphine during the pre-treatment period significantly reduces the signs of withdrawal symptoms, the enhancement of NA turnover, the increase in cyclic AMP and the Fos expression. However, these inhibitors did not modify the levels of cyclic GMP. These findings demonstrated that co-administration of rolipram or diazepam with morphine abolish the development of morphine dependence and suggest that these compounds prevent the up-regulation of the cyclic AMP pathway and the associated increase in cyclic AMP level after naloxone administration.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>González-Cuello</LastName><ForeName>Ana</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Pharmacology, University School of Medicine, 30100 Murcia, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sánchez</LastName><ForeName>Lorenzo</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Hernández</LastName><ForeName>Jesús</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Teresa Castells</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Victoria Milanés</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Laorden</LastName><ForeName>M Luisa</ForeName><Initials>ML</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2007</Year><Month>06</Month><Day>09</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Eur J Pharmacol</MedlineTA><NlmUniqueID>1254354</NlmUniqueID><ISSNLinking>0014-2999</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D058988">Phosphodiesterase 4 Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010726">Phosphodiesterase Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016760">Proto-Oncogene Proteins c-fos</NameOfSubstance></Chemical><Chemical><RegistryNumber>0J45DE6B88</RegistryNumber><NameOfSubstance UI="D009647">Normetanephrine</NameOfSubstance></Chemical><Chemical><RegistryNumber>E0399OZS9N</RegistryNumber><NameOfSubstance UI="D000242">Cyclic AMP</NameOfSubstance></Chemical><Chemical><RegistryNumber>H2D2X058MU</RegistryNumber><NameOfSubstance UI="D006152">Cyclic GMP</NameOfSubstance></Chemical><Chemical><RegistryNumber>K676NL63N7</RegistryNumber><NameOfSubstance UI="D020889">Rolipram</NameOfSubstance></Chemical><Chemical><RegistryNumber>Q3JTX2Q7TU</RegistryNumber><NameOfSubstance UI="D003975">Diazepam</NameOfSubstance></Chemical><Chemical><RegistryNumber>X4W3ENH1CV</RegistryNumber><NameOfSubstance UI="D009638">Norepinephrine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000242" MajorTopicYN="N">Cyclic AMP</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006152" MajorTopicYN="N">Cyclic GMP</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003975" MajorTopicYN="N">Diazepam</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009021" MajorTopicYN="N">Morphine Dependence</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009206" MajorTopicYN="N">Myocardium</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009638" MajorTopicYN="N">Norepinephrine</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009647" MajorTopicYN="N">Normetanephrine</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D058988" MajorTopicYN="N">Phosphodiesterase 4 Inhibitors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010726" MajorTopicYN="N">Phosphodiesterase Inhibitors</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016760" MajorTopicYN="N">Proto-Oncogene Proteins c-fos</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017207" MajorTopicYN="N">Rats, Sprague-Dawley</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020889" MajorTopicYN="N">Rolipram</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013375" MajorTopicYN="N">Substance Withdrawal Syndrome</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2006</Year><Month>12</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2007</Year><Month>5</Month><Day>8</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2007</Year><Month>5</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2007</Year><Month>7</Month><Day>3</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2007</Year><Month>12</Month><Day>6</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2007</Year><Month>7</Month><Day>3</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">17601555</ArticleId><ArticleId IdType="doi">10.1016/j.ejphar.2007.05.051</ArticleId><ArticleId IdType="pii">S0014-2999(07)00627-9</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">17601035</PMID><DateCompleted><Year>2007</Year><Month>08</Month><Day>27</Day></DateCompleted><DateRevised><Year>2016</Year><Month>10</Month><Day>20</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0869-6047</ISSN><JournalIssue CitedMedium="Print"><Issue>5</Issue><PubDate><Year>2007</Year></PubDate></JournalIssue><Title>Vestnik Rossiiskoi akademii meditsinskikh nauk</Title><ISOAbbreviation>Vestn Ross Akad Med Nauk</ISOAbbreviation></Journal>[Long-term results of low-speed irrigated radiofrequency catheter ablation of atrial flutter].
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In this study, we investigated whether morphine dependence was inhibited by phosphodiesterase (PDE) 4 inhibitors rolipram and diazepam, since a role for the cyclic AMP systems in the development of morphine dependence was reported. Dependence of morphine was induced by a 7-day s.c. implantation of morphine pellets. Morphine withdrawal was precipitated on day 8 by an injection of naloxone. In order to determine the effect of rolipram or diazepam the animals were injected with these drugs for seven days and 30 min before the administration of naloxone. When opioid withdrawal was precipitated, enhancement of noradrenaline (NA) turnover in the heart was observed 30 min after naloxone administration. Moreover, morphine withdrawal induces Fos expression, increase in cyclic AMP and cyclic GMP levels. Co-administration of rolipram or diazepam with morphine during the pre-treatment period significantly reduces the signs of withdrawal symptoms, the enhancement of NA turnover, the increase in cyclic AMP and the Fos expression. However, these inhibitors did not modify the levels of cyclic GMP. These findings demonstrated that co-administration of rolipram or diazepam with morphine abolish the development of morphine dependence and suggest that these compounds prevent the up-regulation of the cyclic AMP pathway and the associated increase in cyclic AMP level after naloxone administration.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>González-Cuello</LastName><ForeName>Ana</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Pharmacology, University School of Medicine, 30100 Murcia, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sánchez</LastName><ForeName>Lorenzo</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Hernández</LastName><ForeName>Jesús</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Teresa Castells</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Victoria Milanés</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Laorden</LastName><ForeName>M Luisa</ForeName><Initials>ML</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2007</Year><Month>06</Month><Day>09</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Eur J Pharmacol</MedlineTA><NlmUniqueID>1254354</NlmUniqueID><ISSNLinking>0014-2999</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D058988">Phosphodiesterase 4 Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010726">Phosphodiesterase Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016760">Proto-Oncogene Proteins c-fos</NameOfSubstance></Chemical><Chemical><RegistryNumber>0J45DE6B88</RegistryNumber><NameOfSubstance UI="D009647">Normetanephrine</NameOfSubstance></Chemical><Chemical><RegistryNumber>E0399OZS9N</RegistryNumber><NameOfSubstance UI="D000242">Cyclic AMP</NameOfSubstance></Chemical><Chemical><RegistryNumber>H2D2X058MU</RegistryNumber><NameOfSubstance UI="D006152">Cyclic GMP</NameOfSubstance></Chemical><Chemical><RegistryNumber>K676NL63N7</RegistryNumber><NameOfSubstance UI="D020889">Rolipram</NameOfSubstance></Chemical><Chemical><RegistryNumber>Q3JTX2Q7TU</RegistryNumber><NameOfSubstance UI="D003975">Diazepam</NameOfSubstance></Chemical><Chemical><RegistryNumber>X4W3ENH1CV</RegistryNumber><NameOfSubstance UI="D009638">Norepinephrine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000242" MajorTopicYN="N">Cyclic AMP</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006152" MajorTopicYN="N">Cyclic GMP</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003975" MajorTopicYN="N">Diazepam</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009021" MajorTopicYN="N">Morphine Dependence</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009206" MajorTopicYN="N">Myocardium</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009638" MajorTopicYN="N">Norepinephrine</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009647" MajorTopicYN="N">Normetanephrine</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D058988" MajorTopicYN="N">Phosphodiesterase 4 Inhibitors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010726" MajorTopicYN="N">Phosphodiesterase Inhibitors</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016760" MajorTopicYN="N">Proto-Oncogene Proteins c-fos</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017207" MajorTopicYN="N">Rats, Sprague-Dawley</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020889" MajorTopicYN="N">Rolipram</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013375" MajorTopicYN="N">Substance Withdrawal Syndrome</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2006</Year><Month>12</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2007</Year><Month>5</Month><Day>8</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2007</Year><Month>5</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2007</Year><Month>7</Month><Day>3</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2007</Year><Month>12</Month><Day>6</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2007</Year><Month>7</Month><Day>3</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">17601555</ArticleId><ArticleId IdType="doi">10.1016/j.ejphar.2007.05.051</ArticleId><ArticleId IdType="pii">S0014-2999(07)00627-9</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">17601035</PMID><DateCompleted><Year>2007</Year><Month>08</Month><Day>27</Day></DateCompleted><DateRevised><Year>2016</Year><Month>10</Month><Day>20</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0869-6047</ISSN><JournalIssue CitedMedium="Print"><Issue>5</Issue><PubDate><Year>2007</Year></PubDate></JournalIssue><Title>Vestnik Rossiiskoi akademii meditsinskikh nauk</Title><ISOAbbreviation>Vestn Ross Akad Med Nauk</ISOAbbreviation></Journal><ArticleTitle>[Long-term results of low-speed irrigated radiofrequency catheter ablation of atrial flutter].</ArticleTitle><Pagination><StartPage>11</StartPage><EndPage>19</EndPage><MedlinePgn>11-9</MedlinePgn></Pagination><Abstract>The authors studied long-term results of low-speed (10 ml/min) irrigated radiofrequency catheter ablation (RFA) of the lower isthmus (LI) in patients with typical atrial flutter (AF). This treatment was based upon combined use of local and indirect criteria of the block of isthmus conduction. The influence of RFA LI on quality of life (QL), echocardiographic parameters and cardiac rhythm variability (CRV) was studied. Low-speed irrigated RFA LI, based upon combined use of local and indirect criteria for verification of complete bidirectional blockade in this area, is an effective and safe method of treatment of patients with different variants of clinical course of typical AF which makes it possible to significantly improve QL characteristics and central hemodynamic parameters, and normalize CVR parameters as well. Self-organization of chaos, which realizes according to RR interval time rows, in patients with typical AF after RFA LI may be considered an additional criterion of the effectiveness of this operative intervention and a prognostic sign that predicts maintenance of sinus rhythm in this category of patients.
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2,333,132 |
Evaluation of anaesthesia methods in caesarean section for foetal distress.
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The purpose of this study was to evaluate the anaesthetic technique for Caesarean section which was appropriate for the clinical situation. This retrospective study was conducted on 240 patients undergoing Caesarean section with indications of foetal distress during a 3-year period (2002-2004). The data were reviewed from the patient's medical record of the Department of Anesthesiology, Dr Soetomo Hospital, Surabaya. The patients were divided into three groups, according to the criteria of foetal heart rates. The success of the anaesthesia methods was determined by assessing the Apgar scores of the newborn baby. The results were analyse using Kruskal-Wallis and Chi-Square test. P ≤0.05 was considered as statistically significant. 1- and 5-minute Apgar score of the normal range group was significantly higher than that of the bradycardia group (p<0.05), but no significant differences was found between the normal range and the tachycardia group (p>0.05). One- and five- minute Apgar scores of the sub-arachnoid block group were significantly higher than those of the general anesthesia group (p<0.05). One-minute Apgar score of the ketamine group was significantly higher than that of the thiopental group (p<0.05), but no significant differences in 5-minute Apgar score was found between the ketamine and the thiopental groups (p>0.05). We conclude that subarachnoid block is the choice of anaesthesia for patients undergoing Caesarean section for foetal distress's diagnosed at PS 1 and 2 patients. General anaesthesia with ketamine Apgar score at one minute better than that of the thiopental.
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2,333,133 |
A transcription-dependent mechanism, akin to that in adipose tissue, modulates lipoprotein lipase activity in rat heart.
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The enzyme lipoprotein lipase (LPL) releases fatty acids from lipoprotein triglycerides for use in cell metabolism. LPL activity is rapidly modulated in a tissue-specific manner. Recent studies have shown that in rat adipose tissue this occurs by a shift of extracellular LPL toward an inactive form catalyzed by an LPL-controlling protein whose expression changes in response to the nutritional state. To explore whether a similar mechanism operates in other tissues we injected actinomycin D to block transcription of the putative LPL controlling protein(s). When actinomycin was given to fed rats, heparin-releasable LPL activity increased by 160% in heart and by 150% in a skeletal muscle (soleus) in 6 h. Postheparin LPL activity in blood increased by about 200%. To assess the state of extracellular LPL we subjected the spontaneously released LPL in heart perfusates to chromatography on heparin-agarose, which separates the active and inactive forms of the lipase. The amount of lipase protein released remained relatively constant on changes in the nutritional state and/or blockade of transcription, but the distribution between the active and inactive forms changed. Less of the LPL protein was in the active form in perfusates from hearts from fed compared with fasted rats. When glucose was given to fasted rats the proportion of LPL protein in the active form decreased. Actinomycin D increased the proportion that was active, in accord with the hypothesis that the message for a rapidly turning over LPL-controlling protein was being removed.
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2,333,134 |
Simulations of propagated mouse ventricular action potentials: effects of molecular heterogeneity.
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The molecular heterogeneity of repolarizing currents produces significant spatial heterogeneity and/or dispersion of repolarization in many mammalian cardiac tissues. Transgenic mice are prominent experimental models for the study of the molecular basis of repolarization and arrhythmias. However, it is debated whether the small mouse heart can sustain physiologically relevant heterogeneity of repolarization. We used a comprehensive model of the mouse action potential (AP) to predict how small a region of the cardiac tissue can maintain spatial gradients of repolarization due to differential expression of channels. Our simulations of a one-dimensional multicellular ring or cable predict that substantial gradients in repolarization and intracellular Ca(2+) concentration transients can be maintained through heterogeneity of expression of K(+) channels in distances of approximately 10 cells that are sufficient to block propagation. The abruptness of expression gradients and the site of stimulation can cause Ca(2+) transient oscillations and affect the stability of Ca(2+) dynamics and AP propagation. Two different mechanisms of instability of AP propagation in one-dimensional cable occur at fast pacing rates. Transitions from periodic activity to alternans or to irregular behavior were observed. Abrupt gradients of channel expression can cause alternans at slower pacing rates than gradual changes. Our simulations demonstrate the importance of incorporating realistic Ca(2+) dynamics and current densities into models of propagated AP. They also emphasize that microscopic aspects of tissue organization are important for predicting large-scale propagation phenomena. Finally, our results predict that the mouse heart should be able to sustain substantial molecularly based heterogeneity of repolarization.
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2,333,135 |
Isoform-selective effects of isoflurane on voltage-gated Na+ channels.
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Voltage-gated Na channels modulate membrane excitability in excitable tissues. Inhibition of Na channels has been implicated in the effects of volatile anesthetics on both nervous and peripheral excitable tissues. The authors investigated isoform-selective effects of isoflurane on the major Na channel isoforms expressed in excitable tissues.</AbstractText>Rat Nav1.2, Nav1.4, or Nav1.5 alpha subunits heterologously expressed in Chinese hamster ovary cells were analyzed by whole cell voltage clamp recording. The effects of isoflurane on Na current activation, inactivation, and recovery from inactivation were analyzed.</AbstractText>The cardiac isoform Nav1.5 activated at more negative potentials (peak INa at -30 mV) than the neuronal Nav1.2 (0 mV) or skeletal muscle Nav1.4 (-10 mV) isoforms. Isoflurane reversibly inhibited all three isoforms in a concentration- and voltage-dependent manner at clinical concentrations (IC50 = 0.70, 0.61, and 0.45 mm, respectively, for Nav1.2, Nav1.4, and Nav1.5 from a physiologic holding potential of -70 mV). Inhibition was greater from a holding potential of -70 mV than from -100 mV, especially for Nav1.4 and Nav1.5. Isoflurane enhanced inactivation of all three isoforms due to a hyperpolarizing shift in the voltage dependence of steady state fast inactivation. Inhibition of Nav1.4 and Nav1.5 by isoflurane was attributed primarily to enhanced inactivation, whereas inhibition of Nav1.2, which had a more positive V1/2 of inactivation, was due primarily to tonic block.</AbstractText>Two principal mechanisms contribute to Na channel inhibition by isoflurane: enhanced inactivation due to a hyperpolarizing shift in the voltage dependence of steady state fast inactivation (Nav1.5 approximately Nav1.4 > Nav1.2) and tonic block (Nav1.2 > Nav1.4 approximately Nav1.5). These novel mechanistic differences observed between isoforms suggest a potential pharmacologic basis for discrimination between Na channel isoforms to enhance anesthetic specificity.</AbstractText>
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2,333,136 |
Anti-CD25 treatment and FOXP3-positive regulatory T cells in heart transplantation.
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The interleukin-2 receptor alpha chain (IL-2Ra, CD25) plays a major part in shaping the dynamics of T cell populations following immune activation, due to its role in T cell proliferation and survival. Strategies to blunt the effector responses in transplantation have been developed by devising pharmaceutical agents to block the IL-2 pathways. However, such strategies could adversely affect the CD25(+)FOXP3(+)T regulatory (T reg) populations which also rely on intereukin-2 signaling for survival. The present study shows that a cohort of heart allograft recipients treated with Daclizumab (a humanized anti-CD25 antibody) display FOXP3 expression patterns consistent with functional T regulatory cell populations. High levels of FOXP3 were observed to correlate with lower incidence of and recovery from acute rejection, as well as lower levels of anti-donor HLA antibody production. Therefore, T reg populations appear fully functional in patients treated with Daclizumab, even when 5 doses were administered. By comparison, patients treated with fewer doses or no Daclizumab had a higher incidence of acute rejection, antibody production and graft failure. Therefore, our data indicates that Daclizumab treatment does not interfere with the generation of regulatory T cells and has a beneficial effect on heart allograft survival.
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2,333,137 |
Role of topical calcineurin inhibitors on atopic dermatitis of children.
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Besides the traditional topical treatment of mild and moderate forms of atopic dermatitis (AD), which includes the daily use of emollients and the intermittent use of topical corticosteroids (TCSs) as anti-inflammatory drugs, a new group of drugs has recently been introduced to control the inflammatory phase of the disease: topical calcineurin inhibitors (TCIs). Although the efficacy of TCSs is evident, prolonged unrestricted use is limited by local and systemic side effects. The major risk in children is the hypothalamic-pituitary-adrenal gland suppression, due to the higher percutaneous absorption of the TCSs. TCIs selectively block the activity of calcineurin, a serin/threonine protein phosphatase regulated by cellular calcium first detected in skeletal muscle and brain. Within the past few years, calcineurin has been implicated in a wide range of biological responses including lymphocyte activation, neuronal and muscle development, and morphogenesis of heart valves. TCIs disrupt the intracellular signalling towards NF-AT by forming a complex with macrophilin-12. This complex inhibits the activity of calcineurin, thereby preventing the dephosphorylation of NF-AT and so interfering with the transcription of several genes. The nuclear component of NF-AT, binding to its nuclear counterpart, is essential for the transcription of various genes, including interleukin (IL)-2 and other proinflammatory cytokines. Recent findings about the therapeutic efficacy of TCIs have provided a possible alternative to TCSs in the treatments of mild to severe forms of AD.
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2,333,138 |
Temporal variability of repolarization in rat ventricular myocytes paced with time-varying frequencies.
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Adaptation of action potential duration (APD) to pacing cycle length (CL) has been previously characterized in isolated cardiomyocytes for sudden changes in constant CL and for pre-/postmature stimuli following constant pacing trains. However, random fluctuations characterize both physiological sinus rhythm (up to 10% of mean CL) and intrinsic beat-to-beat APD at constant pacing rate. We analysed the beat-to-beat sensitivity of each APD to the preceding CL during constant-sudden, random or linearly changing pacing trains in single patch clamped rat left ventricular myocytes, in the absence of the autonomic and electrotonic effects that modulate rate dependency in the intact heart. Beat-to-beat variability of APD at -60 mV (APD(-60 mV)), quantified as S.D. over 10-beat sequences, increased with corresponding mean APD. When measured as coefficient of variability (CV), APD(-60 mV) variability was inversely proportional to pacing frequency (from 1.2% at 5 Hz to 3.2% at 0.2 Hz). It was increased, at a basic CL (BCL) of 250 ms, by 55% by the L-type calcium current (I(CaL)) blocker nifedipine, and decreased by 23% by the transient-outward potassium current (I(to)) blocker 4-aminopyridine. Variability of APD at BCL of 250 ms prevented the detection of random changes of CL smaller than approximately 5%. Ten per cent random changes in CL were detected as a 40% increase in CV of APD and tended to correlate with it (r = 0.43). Block of I(CaL) depressed this correlation (r = 0.23), whereas block of I(to) significantly increased it (r = 0.67); this was similar with linearly changing CL ramps (ranging +/-10% and +/-20% of 250 ms). We conclude that beat-to-beat APD variability, a major determinant of the propensity for development of arrhythmia in the heart, is present in isolated myocytes, where it is dependent on mean APD and pacing rate. Action potential duration shows a beat-to-beat positive correlation with preceding randomly/linearly changing CL, which can be pharmacologically modulated.
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2,333,139 |
Haemodynamic effects of intrathecal bupivacaine for surgical repair of hip fracture.
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To determine the optimal dose of bupivacaine in providing adequate surgical anaesthesia with minimal haemodynamic disturbances.</AbstractText>Three different doses of spinal bupivacaine in combination with or without fentanyl for surgical repair of hip fracture were used. Sixty patients were randomly divided into three groups (A, B and C) to receive a spinal anaesthetic of bupivacaine 10mg, 8mg and 6mg respectively. In addition to bupivacaine, group B and C also received fentanyl 20 microg in spinal mixture.</AbstractText>Intra operative heart rate was statistically insignificant in all three groups. Statistically significant drop in systolic blood pressure was found in group A & B at different study timings while statistically significant drop in diastolic blood pressure was only found in group A. Sensory block characteristics were similar among all three groups. Motor block pattern was found marginally significant in group C with highest time to achieve desired block. All patients had satisfactory level of surgical anaesthesia.</AbstractText>This study concluded that low dose, 6 mg bupivacaine with 20 microg fentanyl provide adequate anaesthesia for surgical repair of hip fracture with stable haemodynamics.</AbstractText>
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2,333,140 |
Embryonic cardiac arrhythmia and generation of reactive oxygen species: common teratogenic mechanism for IKr blocking drugs.
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In the adult organism, it is well established that hypoxia followed by reperfusion may be fatal and result in generation of reactive oxygen species (ROS) and subsequent tissue damage. There is also considerable evidence that temporary decrease or interruption in oxygen supply to the embryo and ROS generation during reperfusion result in tissue damage in embryonic tissues. A wide spectrum of different malformations by transient embryonic hypoxia could be produced, depending on the duration, extent, and timing of the hypoxic event. It is the contention of this paper that drugs that block the potassium channel IKr, either as an intended pharmacologic effect or as an unwanted side-effect, are potentially teratogenic by a common ROS related mechanism. Drugs blocking the IKr channel, such as almokalant, dofetilide, phenytoin, cisapride and astemizole, do all produce a similar pattern of hypoxia-related malformations. Mechanistic studies show that the malformations are preceded by embryonic cardiac arrhythmia and periods of hypoxia/reoxygenation in embryonic tissues. Pretreatment or simultaneous treatment with radical scavengers with capacity to capture ROS, markedly decrease the teratogenicity of different IKr blocking drugs. A second aim of this review is to demonstrate that the conventional design of teratology studies is not optimal to detect malformations caused by IKr blocking drugs. Repeated high doses result in high incidences of embryonic death due embryonic cardiac arrhythmia, thus masking their teratogenic potential. Instead, single dosing on specific days is proposed to be a better way to characterize the teratogenic potential of Ikr blocking drugs.
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2,333,141 |
Sub-plasmalemmal [Ca2+]i upstroke in myocytes of the guinea-pig small intestine evoked by muscarinic stimulation: IP3R-mediated Ca2+ release induced by voltage-gated Ca2+ entry.
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Membrane depolarization triggers Ca(2+) release from the sarcoplasmic reticulum (SR) in skeletal muscles via direct interaction between the voltage-gated L-type Ca(2+) channels (the dihydropyridine receptors; VGCCs) and ryanodine receptors (RyRs), while in cardiac muscles Ca(2+) entry through VGCCs triggers RyR-mediated Ca(2+) release via a Ca(2+)-induced Ca(2+) release (CICR) mechanism. Here we demonstrate that in phasic smooth muscle of the guinea-pig small intestine, excitation evoked by muscarinic receptor activation triggers an abrupt Ca(2+) release from sub-plasmalemmal (sub-PM) SR elements enriched with inositol 1,4,5-trisphosphate receptors (IP(3)Rs) and poor in RyRs. This was followed by a lesser rise, or oscillations in [Ca(2+)](i). The initial abrupt sub-PM [Ca(2+)](i) upstroke was all but abolished by block of VGCCs (by 5 microM nicardipine), depletion of intracellular Ca(2+) stores (with 10 microM cyclopiazonic acid) or inhibition of IP(3)Rs (by 2 microM xestospongin C or 30 microM 2-APB), but was not affected by block of RyRs (by 50-100 microM tetracaine or 100 microM ryanodine). Inhibition of either IP(3)Rs or RyRs attenuated phasic muscarinic contraction by 73%. Thus, in contrast to cardiac muscles, excitation-contraction coupling in this phasic visceral smooth muscle occurs by Ca(2+) entry through VGCCs which evokes an initial IP(3)R-mediated Ca(2+) release activated via a CICR mechanism.
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2,333,142 |
Activation of MAPK in hearts of EMD null mice: similarities between mouse models of X-linked and autosomal dominant Emery Dreifuss muscular dystrophy.
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Emery-Dreifuss muscular dystrophy (EDMD) is an inherited disorder characterized by slowly progressive skeletal muscle weakness in a humero-peroneal distribution, early contractures and prominent cardiomyopathy with conduction block. Mutations in EMD, encoding emerin, and LMNA, encoding A-type lamins, respectively, cause X-linked and autosomal dominant EDMD. Emerin and A-type lamins are proteins of the inner membrane of the nuclear envelope. Whereas the genetic cause of EDMD has been described and the proteins well characterized, little is known on how abnormalities in nuclear envelope proteins cause striated muscle disease. In this study, we analyzed genome-wide expression profiles in hearts from Emd knockout mice, a model of X-linked EDMD, using Affymetrix GeneChips. This analysis showed a molecular signature similar to that we previously described in hearts from Lmna H222P knock-in mice, a model of autosomal dominant EDMD. There was a common activation of the ERK1/2 branch of the mitogen-activated protein kinase (MAPK) pathway in both murine models, as well as activation of downstream targets implicated in the pathogenesis of cardiomyopathy. Activation of MAPK signaling appears to be a cornerstone in the development of heart disease in both X-linked and autosomal dominant EDMD.
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2,333,143 |
Elevated Ca2+ ATPase (SERCA2) activity in tuna hearts: comparative aspects of temperature dependence.
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Tunas have an extraordinary physiology including elevated metabolic rates and high cardiac performance. In some species, retention of metabolic heat warms the slow oxidative swimming muscles and visceral tissues. In all tunas, the heart functions at ambient temperature. Enhanced rates of calcium transport in tuna myocytes are associated with increased expression of proteins involved in the contraction-relaxation cycle. The cardiac SR Ca2+-ATPase (SERCA2) plays a major role during cardiac excitation-contraction (E-C) coupling. Measurements of oxalate-supported Ca2+-uptake in atrial SR vesicles isolated from four species of tunas indicate that bluefin have at least two fold higher Ca2+-uptake than all other tunas examined between 5 and 30 degrees C. The highest atrial Ca2+-uptake was measured in bluefin tuna at 30 degrees C (23.32+/-1.58 nmol Ca2+/mg/min). Differences among tunas in the temperature dependency of Ca2+-uptake were similar for ATP hydrolysis. Western blot analysis revealed a significant increase in SERCA2 content associated with higher Ca2+ uptake rates in the atrial tissues of bluefin tuna and similar RyR expression across species. We propose that the expression of EC coupling proteins in cardiac myocytes, and the higher rates of SERCA2 activity are an important evolutionary step for the maintenance of higher heart rates and endothermy in bluefin tuna.
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2,333,144 |
The vicissitudes of the pacemaker current I (Kdd) of cardiac purkinje fibers.
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The mechanisms underlying the pacemaker current in cardiac tissues is not agreed upon. The pacemaker potential in Purkinje fibers has been attributed to the decay of the potassium current I (Kdd). An alternative proposal is that the hyperpolarization-activated current I (f) underlies the pacemaker potential in all cardiac pacemakers. The aim of this review is to retrace the experimental development related to the pacemaker mechanism in Purkinje fibers with reference to findings about the pacemaker mechanism in the SAN as warranted. Experimental data and their interpretation are critically reviewed. Major findings were attributed to K(+) depletion in narrow extracellular spaces which would result in a time dependent decay of the inward rectifier current I (K1). In turn, this decay would be responsible for a "fake" reversal of the pacemaker current. In order to avoid such a postulated depletion, Ba(2+) was used to block the decay of I (K1). In the presence of Ba(2+) the time-dependent current no longer reversed and instead increased with time and more so at potentials as negative as -120 mV. In this regard, the distinct possibility needs to be considered that Ba(2+) had blocked I (Kdd) (and not only I (K1)). That indeed this was the case was demonstrated by studying single Purkinje cells in the absence and in the presence of Ba(2+). In the absence of Ba(2+), I (Kdd) was present in the pacemaker potential range and reversed at E (K). In the presence of Ba(2+), I (Kdd) was blocked and I (f) appeared at potentials negative to the pacemaker range. The pacemaker potential behaves in a manner consistent with the underlying I (Kdd) but not with I (f). The fact that I (f) is activated on hyperpolarization at potential negative to the pacemaker range makes it suitable as a safety factor to prevent the inhibitory action of more negative potentials on pacemaker discharge. It is concluded that the large body of evidence reviewed proves the pacemaker role of I (Kdd) (but not of I (f)) in Purkinje fibers.
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2,333,145 |
Sevoflurane increases fade of neuromuscular response to TOF stimulation following rocuronium administration in children. A PK/PD analysis.
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Sevoflurane enhances neuromuscular block produced by rocuronium, affecting not only single twitch response but also the response to high-frequency stimulation, increasing tetanic [or train-of-four (TOF)] fade.</AbstractText>We compared the degree of fade during spontaneous recovery from rocuronium-induced neuromuscular block in 24 children (3-11 years old, ASA groups I and II), anesthetized with nitrous oxide-sevoflurane (one MAC, endtidal concentration) or nitrous oxide-fentanyl. Neuromuscular transmission was monitored electromyographically (EMG), stimulating the ulnar nerve at the wrist with TOF, 2 Hz for 2 s, repeated at 20-s intervals and recording EMG potential from adductor pollicis brevis. Depression of the fourth twitch, T4, was used as a measure of fade. Following an intubating dose of rocuronium, 0.6 mgxkg(-1), continuous infusion of rocuronium was given to maintain stable 90-99% T1 depression. Plasma concentration of rocuronium was determined with high performance liquid chromatography with electrochemical detection (HPLC-EC) method at the moment of discontinuation of rocuronium infusion and 10, 20, 30, 40, 50, 60, and 75 min afterwards. A two compartment model was used for pharmacokinetic (PK) calculations. PK parameters were fixed and pharmacodynamic data were fitted to effect compartment model proposed by Sheiner.</AbstractText>Sevoflurane reduced rocuronium concentration in effect compartment producing 50% inhibition of both T1 and T4 response and significantly delayed not only T1, but also T4 recovery.</AbstractText>Potentiating effect of sevoflurane on rocuronium-induced neuromuscular block influences not only postsynaptic, but also the presynaptic part of the neuromuscular junction, enhancing fade of neuromuscular response to high-frequency stimulation. The intensity of this latter effect is clinically relevant.</AbstractText>
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2,333,146 |
Effects of oral cocaine on intravenous cocaine discrimination in humans.
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This study was designed to evaluate the drug discrimination paradigm as a model for assessing the ability of potential agonist medications to block the effects of intravenous cocaine. Previous research has demonstrated that oral cocaine attenuated the subjective and physiological effects of intravenous cocaine injections, and in the absence of a known efficacious medication for cocaine use disorders, a proof-of-concept approach was used in which cocaine was acutely administered orally to block intravenous cocaine's discriminative-stimulus effects. During training, 11 cocaine-dependent participants were able to discriminate between intravenous saline and 20 mg/70 kg iv cocaine, and 8 of these participants completed the study. After training, participants ingested capsules containing either placebo or 300 mg/70 kg cocaine 60 min prior to the intravenous injection of different doses of cocaine during test sessions with no contingencies in place. Each cocaine dose was administered twice, once under each oral pretreatment condition. Training sessions were interspersed among the test sessions. Physiological and subjective effects were measured throughout each session. Oral cocaine moderately increased some of the subjective and physiological effects of the lower doses of intravenous cocaine, whereas effects at the higher doses were unaltered. Similar changes were seen for the discrimination results. Thus, although oral cocaine given acutely likely is not a viable treatment medication for cocaine dependence, the usefulness of the drug discrimination model in the evaluation of agonist treatment medications remains unclear.
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2,333,147 |
The guestbook of the urology department of Semmelweis University in Budapest: a mirror of international contacts.
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The Department of Urology at Semmelweis University, Budapest was established in 1920 as one of the first independent urological clinics in Europe. The history of the guestbook begins in 1922 with Professor Illyés, the first appointed head of the department.</AbstractText>Information was collected on the most famous urologists from those times, who were mostly working in the United States. In addition, guests from around the world were grouped according to the countries from which they came, highlighting the political situation of those times in Hungary.</AbstractText>Before World War II guests mostly came from the United States and a few other countries. However, after World War II almost no Western European or American guests visited, but there were still many urologist visitors from the Soviet Union and Eastern block countries. With a slight political improvement in 1961 Western European and American urologists increased visits to the department. Since 1997 Professor Imre Romics has been the department chair, and has seen the greatest number of visitors from around the world.</AbstractText>The guestbook of the Semmelweis University Department of Urology is a real mirror of international contacts, and represents the last few decades of history of a country in the heart of middle Europe.</AbstractText>
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2,333,148 |
Impact of tobacco-smoke on key signaling pathways in the innate immune response in lung macrophages.
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Many of the healthcare consequences of cigarette smoking could be due to its ability to compromise the immune system, and in respiratory diseases like chronic obstructive pulmonary disease (COPD), a constant low level of infection could be responsible for some of the symptoms/pathology. The aim was to assess the impact of cigarette smoke (CS) on the release of innate effector cytokines in THP-1 cells and human lung macrophages, and to determine the molecular mechanism behind the altered response. Cells were exposed to CS with and without endotoxin stimulus, cytokines, glutathione, mitogen-activated protein kinase (MAPK) phosphorylation, IkappaB kinase-2 (IKK-2) activity, nuclear factor kappa B (NF-kappaB), and activator protein-1 (AP-1) pathway activation was measured. Attempts were made to mimic or block the effect of CS by using nicotine, nitric oxide donors/inhibitors, prostanoid inhibitors, and anti-oxidants. Results showed that CS initially delayed the production of "innate" cytokines (e.g., IL-1beta and IL-6) and reduced glutathione levels. This was associated with a reduction in NF-kappaB pathway activation, which suggested a causative link. CS also increased the phosphorylation of MAPK's and the production of IL-8 but interestingly only in stimulated cells. Exogenous glutathione treatment reversed both these effects of CS, which suggests that this molecule may play a central role. In conclusion, this data provides a novel mechanistic explanation for why smokers have increased prevalence/severity of respiratory infections. In addition, the suppression of the innate response is accompanied by an increase in the neutrophil chemoattractant, IL-8, which may suggest a link to the pathogenesis of smoking-related inflammatory disease.
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2,333,149 |
Thrombin formation in vitro in response to shear-induced activation of platelets.
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Thromboembolic events caused by implanted vascular devices present serious medical challenges. In particular bileaflet mechanical heart valves (MHVs) are prone to thrombus formation in the hinge region due to a combination of high shear stress and stagnation regions. Most studies of shear-induced platelet activation and aggregation have been performed using viscometers, parallel plate flow, and other non-physiologic in vitro configurations. The present study investigated these events in a physiogically relevant environment in which thrombin formation in response to shear stress activation of platelets plays a more predominant role.</AbstractText>Anticoagulated (citrated) human blood was placed in a steady flow loop containing a 400 microm round orifice or various MHVs in the leakage position. Simultaneous blood recalcification enhanced the thrombus forming potential of the blood. Aggrastat and AN51 were used to block binding to the platelet GPIIb/IIIa and GPIb receptors, respectively, and aspirin was used to block thromboxane production. Thrombin generation was measured indirectly by the thrombin-antithrombin III assay.</AbstractText>Aggrastat, AN51, and aspirin all suppressed thrombin formation. Furthermore, histological results suggested important roles for vWF and fibrinogen in a two-step model of thrombus formation. Thus, thrombin is reproducibly formed in this in vitro system, a process that can be suppressed by blocking platelet activation. This system has the potential to investigate mechanisms and interventions for medical devices that contact with blood under varying shear stress conditions.</AbstractText>
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2,333,150 |
Electronic dental anaesthesia for third inferior molar surgery.
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The aim of this study was to evaluate the efficacy of Electronic Dental Anaesthesia (EDA) for third molar surgery.</AbstractText>Third molar extraction under regional anaesthesia (inferior alveolar and buccal nerve blocks) was performed in 2 groups of 30 patients each: group 1 = controls, group 2 = EDA treatment. Anxiety and pain level were reported by means of Visual Analogue Scale, postoperative pain description with the McGill Pain Questionnaire. A postoperative phone interview to all patients was made. Computerized randomization was performed; values expressed as mean+/-SD, data comparison evaluated by means of ANOVA and chi squared, statistical significance indicated by P values <0.05.</AbstractText>Features of the patients and surgical interventions were similar. EDA has determined lower pain level; moreover, the control patients has shown higher values of blood pressure and heart frequency. Phone interview has reported no amnesia about the perioperative events. A smaller number of EDA treated patients has reported pain during needle prick and/or intraoperatively; 80% of the EDA treated patients has reported a good opinion about the treatment, 93% of the patients would repeat the treatment, if needed.</AbstractText>EDA is a complementary analgesic technique for dental surgery. Cardiovascular changes, frequently observed during third molar extraction, were not present in the EDA treated patients. These data confirm that EDA is able to modify the physiologic responses to stressful events, blunting the adrenergic upset, maybe by means of an analgesic action on A, fiber and an increase of endorphins' central level. These results underline that the complementary use of EDA in the third molar extraction may be better than regional anaesthesia alone.</AbstractText>
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2,333,151 |
Eponymous doctors associated with Edinburgh, Part 2--David Bruce, John Cheyne, William Stokes, Alexander Monro Secundus, Joseph Gamgee.
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This, the second in a three-paper series with this title, looks at famous doctors who trained in Edinburgh and their eponyms. With one possible exception, none seems to have sought the eponym, nor awarded it to themselves, nor used it for self-promotion. Unlike those in the first paper, all eponyms in this paper are still in use and their brevity is in contrast to the lengthy description needed if the eponym is not used. Examples are Cheyne-Stokes respiration, Stokes-Adam attacks, Brucellosis and Gamgee dressing. Monro Secundus is included because of his vehement defence of his professional reputation and research findings when he suspected others of trying to detract credit from him, a characteristic seldom reported for the others.
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2,333,152 |
Replacement of nonmuscle myosin II-B with II-A rescues brain but not cardiac defects in mice.
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The purpose of these studies was to learn whether one isoform of nonmuscle myosin II, specifically nonmuscle myosin II-A, could functionally replace a second one, nonmuscle myosin II-B, in mice. To accomplish this, we used homologous recombination to ablate nonmuscle myosin heavy chain (NMHC) II-B by inserting cDNA encoding green fluorescent protein (GFP)-NMHC II-A into the first coding exon of the Myh10 gene, thereby placing GFP-NMHC II-A under control of the endogenous II-B promoter. Similar to B(-)/B(-) mice, most B(a*)/B(a*) mice died late in embryonic development with structural cardiac defects and impaired cytokinesis of the cardiac myocytes. However, unlike B(-)/B(-) mice, 15 B(a*)/B(a*) mice of 172 F2 generation mice survived embryonic lethality but developed a dilated cardiomyopathy as adults. Surprisingly none of the B(a*)/B(a*) mice showed evidence for hydrocephalus that is always found in B(-)/B(-) mice. Rescue of this defect was due to proper localization and function of GFP-NMHC II-A in place of NMHC II-B in a cell-cell adhesion complex in the cells lining the spinal canal. Restoration of the integrity and adhesion of these cells prevents protrusion of the underlying cells into the spinal canal where they block circulation of the cerebral spinal fluid. However, abnormal migration of facial and pontine neurons found in NMHC II-B mutant and ablated mice persisted in B(a*)/B(a*) mice. Thus, although NMHC II-A can substitute for NMHC II-B to maintain integrity of the spinal canal, NMHC II-B plays an isoform-specific role during cytokinesis in cardiac myocytes and in migration of the facial and pontine neurons.
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2,333,153 |
Corticosteroid inhibition of growth-related oncogene protein-alpha via mitogen-activated kinase phosphatase-1 in airway smooth muscle cells.
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Expression of the inflammatory chemokine, growth-related oncogene protein-alpha (GRO-alpha), from airway smooth muscle cells (ASMC) is regulated by pathways involving NF-kappaB and MAPK activation. We determined the effects of dexamethasone on GRO-alpha induced by IL-1beta or TNF-alpha with respect to the role of MAPK pathways and of MAPK phosphatase-1 (MKP-1). Human ASMC were studied in primary culture at confluence. Dexamethasone (10(-8)-10(-5) M) partially inhibited GRO-alpha expression and release induced by IL-1beta and TNF-alpha; this was associated with an inhibition of JNK, but not of p38 or ERK phosphorylation. Together with IL-1beta or TNF-alpha, dexamethasone rapidly induced mRNA and protein expression of MKP-1, which dephosphorylates MAPKs. Using MKP-1 small interfering RNA (siRNA) to block the expression of IL-1beta- and dexamethasone-induced MKP-1 by 50%, JNK phosphorylation was doubled. The inhibitory effect of dexamethasone on GRO-alpha release was partially reversed in ASMC treated with MKP-1 siRNA compared with those treated with scrambled siRNA. In contrast, overexpression of MKP-1 led to a reduction in IL-1beta-induced release of GRO-alpha, but the inhibitory effects of dexamethasone were preserved. Nuclear translocation of the glucocorticoid receptor was increased in ASMC exposed to dexamethasone and IL-1beta. Using chromatin immunoprecipitation assay, glucocorticoid receptor binding to the MKP-1 promoter was increased by IL-1beta and dexamethasone compared with either alone. Glucocorticoids and IL-1beta or TNF-alpha modulate GRO-alpha release partly through the inhibition of JNK pathway, resulting from an up-regulation of MKP-1 expression.
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2,333,154 |
[Levobupivacaine for parturients undergoing elective caesarean delivery. A dose-finding investigation].
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The optimum intrathecal dose of hyperbaric levobupivacaine for spinal anaesthesia during elective caesarean section has not yet been investigated.</AbstractText>A total of 30 parturients undergoing elective caesarean section were included in this prospective, randomised, double-blind study. Parturients received either 7.5, 10 or 12.5 mg hyperbaric 0.5% levobupivacaine intrathecally. Analgesic, sensory and motor block characteristics as well as maternal and fetal levobupivacaine plasma concentrations were determined.</AbstractText>Of the parturients receiving 7.5 mg levobupivacaine 40% required supplementary intravenous opioid analgesics intraoperatively and none achieved complete motor block. Compared to 7.5 mg levobupivacaine, 10 and 12.5 mg significantly prolonged duration of effective analgesia postoperatively (median: 45 vs. 81 and 96 min, respectively). Both maternal and fetal levobupivacaine plasma concentrations were low, with dose-dependent, statistically significant differences in maternal plasma concentrations.</AbstractText>Levobupivacaine 7.5 mg did not provide satisfactory intraoperative analgesia in all parturients. There were no statistically significant differences between 10 and 12.5 mg levobupivacaine with respect to analgesic, sensory and motor block characteristics. Therefore, based on these data, 10 mg levobupivacaine is recommended for parturients undergoing elective caesarean section with spinal anaesthesia.</AbstractText>
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2,333,155 |
The effect of antihistamine cetirizine on ventricular repolarization in congenital long QT syndrome.
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Many drugs are known to block cardiac potassium channels, thus prolonging QT interval and predisposing to malignant arrhythmias. Patients with congenital long QT syndrome are particularly vulnerable, but usually electrophysiological effects of drugs have not been assessed in these patients at risk.</AbstractText>Fifteen asymptomatic patients with type 1 (LQT1), 15 patients with type 2 (LQT2) long QT syndrome, and 15 healthy volunteers took a placebo and cetirizine 10 mg. In addition, healthy volunteers took cetirizine 50 mg. The study was single-blinded and randomized. Exercise tests were performed during stable plasma concentrations. The electrocardiogram was recorded with a body surface potential mapping system (BSPM). Data were analyzed with an automated analyze program. QT intervals to the T wave apex and T wave end and their difference (Tp-e) were determined at rest and at specified heart rates during and after exercise.</AbstractText>Cetirizine did not lengthen the QT intervals at rest or during exercise and recovery in any group. It shortened Tp-e at rest in LQT1 and LQT2 patients and during exercise test in LQT1 patients, thus slightly decreasing electrocardiographic transmural dispersion of repolarization.</AbstractText>Cetirizine does not adversely modify ventricular repolarization in types 1 and 2 long QT syndrome, suggesting that it might be used safely in these long QT syndrome patients.</AbstractText>
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2,333,156 |
Effects of pulsatile blood flow in large vessels on thermal dose distribution during thermal therapy.
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The aim of this study is to evaluate the effect of pulsatile blood flow in thermally significant blood vessels on the thermal lesion region during thermal therapy of tumor. A sinusoidally pulsatile velocity profile for blood flow was employed to simulate the cyclic effect of the heart beat on the blood flow. The evolution of temperature field was governed by the energy transport equation for blood flow together with Pennes' bioheat equation for perfused tissue encircling the blood vessel. The governing equations were numerically solved by a novel multi-block Chebyshev pseudospectral method and the accumulated thermal dose in tissue was computed. Numerical results show that pulsatile velocity profile, with various combinations of pulsatile amplitude and frequency, has little difference in effect on the thermal lesion region of tissue compared with uniform or parabolic velocity profile. However, some minor differences on the thermal lesion region of blood vessel is observed for middle-sized blood vessel. This consequence suggests that, in this kind of problem, we may as well do the simulation simply by a steady uniform velocity profile for blood flow.
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2,333,157 |
Predictors of rehabilitation outcomes: a comparison of Israeli and Italian geriatric post-acute care (PAC) facilities using the minimum data set (MDS).
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To understand the relative contribution of sociodemographic, clinical, and health care features to rehabilitation outcomes in Israel and in Italy in post-acute care (PAC) facilities.</AbstractText>Prospective cross-national study</AbstractText>Two hospital geriatric PAC departments: Harzfeld Geriatric Hospital, Gedera, Israel, and Catholic University of Sacred Heart Geriatric Hospital, Rome, Italy.</AbstractText>Post-acute care patients aged 65 and older admitted consecutively for stabilization, improvement, or rehabilitation to 3 departments in Harzfeld Geriatric Hospital, Gedera, Israel from April, 1999 through February, 2002 (N = 364), and to the post-acute Geriatric Rehabilitation Unit of the "A. Gemelli" Hospital, Catholic University of Sacred Heart, Rome, Italy, between February, 1999, and April, 2002 (N = 351), for whom there were complete assessments at admission and discharge (the total number admitted in Israel was 505, and in Italy, 409).</AbstractText>Minimum Data Set for Post-Acute Care (MDS-PAC) assessments conducted within 4 days of admission and at discharge; data collected identically in both sites. Predictors of functional recovery> were identified using multivariate binary logistic regression. The dependent variable: improvement of 1 or more points in the ADL scale.</AbstractText>The staffing pattern of the PAC department in Italy had about double the physicians and physio- and occupational therapists than in Israel, but about the same number of nurses and somewhat fewer aides than in Israel. Multivariate binary logistic regression that includes country, age, sex, and marital status, found that the patients in Italy had about triple the probability of improvement in ADL function (OR 3.3, CI 2.4-4.6) (P < .001) than PAC patients in Israel. Even after health system characteristics were added to the model, ADL improvement was most significantly associated with higher cognitive ability and a diagnosis of hip fracture, as well as longer length of stay and being admitted to PAC directly from an acute hospital. For each additional point (worse cognition) in a cognitive scale, there was a 30% decrease in the probability of ADL improvement (OR 0.7, CI 0.6-0.8, P < .001). Those who had a stroke were about half as likely to show ADL improvement (OR 0.5, CI 0.3-0.7) than those without stroke, but those with a hip fracture had more than double the probability of ADL improvement (OR 2.7, CI 1.7-4.2) than those without hip fracture. Those who stayed in the PAC ward an additional block of time had a 30% higher probability of ADL improvement (P < .1), and those who were admitted directly to PAC from an acute hospital had more than 4 times the probability of ADL improvement (OR 4.1, CI 2.3-7.0, P < .001) than those who were admitted from a private home.</AbstractText>We found support for the hypothesis that differences in sociodemographic and clinical factors cannot account for all differences in ADL improvement, and that the organization of care and constraints of the health system also influence functional outcomes. Policymakers should examine the policy-amenable features of the Italian and Israeli systems so that optimal ADL recovery can be encouraged. Any reduction in disability will help both patients and the health care system; slightly higher short-term PAC treatment costs may have large long-term future benefits, if they result in the reduction of ADL disability. This study is one of the first to examine outcomes of PAC in 2 countries, and can provide an initial assessment of how rehabilitation can be enhanced or limited by health policies and staffing patterns.</AbstractText>
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2,333,158 |
Is a fall in baseline heart rate a reliable predictor of a successful single shot caudal epidural in children?
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This study was designed to investigate whether a fall in heart rate (HR) with injection of local anesthetic into the caudal space can be used as a predictor of correct needle placement.</AbstractText>Two hundred and twenty pediatric patients undergoing infraumbilical surgery were recruited to the study. After induction of general anesthesia, baseline HR was recorded and caudal block was performed using 0.75-1 ml x kg(-1) 0.25% bupivacaine, which was injected at a rate of 1 ml x 3 s(-1). The change in HR while injecting an initial 0.2 ml x kg(-1) of drug and during total drug injection was recorded. HR reduction of > or = 3 b x min(-1) was considered a positive test for correct needle placement. The success of block was judged by HR response to skin incision, endtidal halothane concentration required for maintenance of anesthesia and postoperative pain scores.</AbstractText>Caudal block was successful in 209/220 (95%) patients. Mean HR following the initial drug injection (111 +/- 17.7, P < 0.01) and entire drug injection (108.8 +/- 17.2, P < 0.01) was significantly lower than baseline (116.2 +/- 17.5). HR reduction of > or = 3 b x min(-1) was present in 190/209 and 199/209 successful block following initial drug injection and total drug injection respectively. The analysis of study data showed that a fall in HR is a predictor of successful caudal block, with a sensitivity of 90.9%, specificity of 100% and a positive predictive value of 100% after initial injection of local anesthetic.</AbstractText>We conclude that decrease in HR with drug injection is a simple, objective and reliable test to predict success of caudal block.</AbstractText>
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2,333,159 |
Effect of cardioactive drugs on action potential generation and propagation in embryonic stem cell-derived cardiomyocytes.
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Extracellular recordings of spontaneous electrical activity in contracting cardiac clusters differentiated from murine embryonic stem cells enable to study electrophysiological features of this in-vitro cardiac-like tissue as well as effects of pharmacological compounds on its chronotropy and electrical conduction. To test if the microelectrode array (MEA) system could serve as a basis for development of a pharmacological screening tool for cardioactive drugs, we used spontaneously beating outgrowths of three-dimensional ES cell aggregates ("embryoid bodies", EBs) plated onto substrate-integrated MEAs. The effects of the L-type Ca(2+) channel antagonist verapamil and Na(+) and K(+) channel blockers (tetrodotoxin, 4-aminopyridine, and sparfloxacin) on the deduced interrelated cardiac network function were investigated. Application of 10(-6) M verapamil led to arrhythmic spiking with a burst-like pattern; at a higher concentration (10(-5) M) the drug caused a sustained negative chronotropy up to complete stop of beating. In the presence of tetrodotoxin a conduction block was observed. Since modulation of K(+) channel activity can cause anti- or proarrhythmic effects, the influence of K(+) channel blockers, namely 4-aminopyridine and sparfloxacin, was investigated. 4-aminopyridine (2x10(-3) M) significantly stabilized beating frequency, while the field potential duration (FPD) was concentration-dependently prolonged up to 2.7-fold. Sparfloxacin (3x10(-6) M) stabilized the beating frequency as well. At a higher concentration of sparfloxacin (3x10(-5) M), a significant prolongation of the spike duration was registered; application of the drug caused also early afterdepolarizations. The results demonstrate a suitability of the studied in-vitro cardiac cell model for pharmacological drug testing in cardiovascular research.
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2,333,160 |
Endogenous and exogenous cardiac glycosides: their roles in hypertension, salt metabolism, and cell growth.
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Cardiotonic steroids (CTS), long used to treat heart failure, are endogenously produced in mammals. Among them are the hydrophilic cardenolide ouabain and the more hydrophobic cardenolide digoxin, as well as the bufadienolides marinobufagenin and telecinobufagin. The physiological effects of endogenous ouabain on blood pressure and cardiac activity are consistent with the "Na(+)-lag" hypothesis. This hypothesis assumes that, in cardiac and arterial myocytes, a CTS-induced local increase of Na(+) concentration due to inhibition of Na(+)/K(+)-ATPase leads to an increase of intracellular Ca(2+) concentration ([Ca(2+)](i)) via a backward-running Na(+)/Ca(2+) exchanger. The increase in [Ca(2+)](i) then activates muscle contraction. The Na(+)-lag hypothesis may best explain short-term and inotropic actions of CTS. Yet all data on the CTS-induced alteration of gene expression are consistent with another hypothesis, based on the Na(+)/K(+)-ATPase "signalosome," that describes the interaction of cardiac glycosides with the Na(+) pump as machinery activating various signaling pathways via intramembrane and cytosolic protein-protein interactions. These pathways, which may be activated simultaneously or selectively, elevate [Ca(2+)](i), activate Src and the ERK1/2 kinase pathways, and activate phosphoinositide 3-kinase and protein kinase B (Akt), NF-kappaB, and reactive oxygen species. A recent development indicates that new pharmaceuticals with antihypertensive and anticancer activities may be found among CTS and their derivatives: the antihypertensive rostafuroxin suppresses Na(+) resorption and the Src-epidermal growth factor receptor-ERK pathway in kidney tubule cells. It may be the parent compound of a new principle of antihypertensive therapy. Bufalin and oleandrin or the cardenolide analog UNBS-1450 block tumor cell proliferation and induce apoptosis at low concentrations in tumors with constitutive activation of NF-kappaB.
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2,333,161 |
Electrical and mechanical effects induced by cold temperatures in the ventricle of isolated Rana ridibunda hearts.
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A temperature decrease changes the contractility of the amphibian heart, but the underlying mechanisms are not totally understood. The objectives of the present work were to better understand the intrinsic mechanisms supporting contractility changes induced by a rapid temperature decrease in the ventricle of Rana ridibunda, and to investigate how fast they develop. Ventricular mechanical cycles (VMCs) and monophasic action potentials (MAPs) recorded from 15 isolated hearts were measured at 15, 30, 45, 60, 90, 120 and 150 s after the application of Ringer solutions of 20, 10 and 5 degrees C. Treatment with 10 and 5 degrees C Ringer solutions decreased the heart rate, and increased the magnitude of the ventricular contraction and the duration of the contraction and relaxation periods. The electrical changes included prolongation of the MAP depolarization plateau, which also decreased in amplitude as an effect of perfusion with 5 degrees C Ringer solution. In addition, treatment with 5 degrees C Ringer solution increased the latency of contraction. The block of L-type channels totally abolished the depolarization plateau at all perfusion temperatures, but failed to inhibit ventricular contraction. In conclusion, treatment with cold temperatures changes the electrical activity of the ventricular myocardium in R. ridibunda hearts, which results in modified ventricular contractility. Data suggest that in addition to L-type Ca2+ channels, other components that support calcium elevation are present R. ridibunda ventricular cells.
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2,333,162 |
Discovery of acetyl-coenzyme A carboxylase 2 inhibitors: comparison of a fluorescence intensity-based phosphate assay and a fluorescence polarization-based ADP Assay for high-throughput screening.
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Acetyl-coenzyme A carboxylase (ACC) enzymes exist as two isoforms, ACC1 and ACC2, which play critical roles in fatty acid biosynthesis and oxidation. Though each isoform differs in tissue and subcellular localization, both catalyze the biotin- and ATP-dependent carboxylation of acetyl-coenzyme A to generate malonyl-coenzyme A, a key metabolite in the control of fatty acid synthesis and oxidation. The cytosolic ACC1 is expressed primarily in liver and adipose tissue, and uses malonyl-coenzyme A as a key building block in fatty acid biosynthesis. The mitochondrial ACC2 is primarily expressed in heart and skeletal muscle, where it is involved in the regulation of fatty acid oxidation. Inhibitors of ACC enzymes may therefore be useful therapeutics for diabetes, obesity, and metabolic syndrome. Two assay formats for these ATP-utilizing enzymes amenable to high-throughput screening are compared: a fluorescence intensity-based assay to detect inorganic phosphate and a fluorescence polarization-based assay to detect ADP. Acetyl-coenzyme A carboxylase inhibitors were identified by these high-throughput screening methods and were confirmed in a radiometric high performance liquid chromatography assay of malonyl-coenzyme A production.
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2,333,163 |
Use of mTOR inhibitors in human organ transplantation.
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The mammalian target of rapamycin (mTOR) inhibitor drugs rapamycin (sirolimus) and everolimus have undergone extensive clinical trials for a variety of organ grafts and have been licensed for use in human transplantation. Uniquely, they block the function of a master chemical switch, the protein kinase mTOR, which integrates the multiple biochemical pathways that are necessary for growth factors to induce cell proliferation. Many of these pathways are abnormal in tumorigenesis, and the role of mTOR and its inhibitors in cancer treatment is undergoing intense investigation. There are pharmacokinetic differences between the rapamycins, however, in all major respects, their actions are the same. They show synergy with the calcineurin inhibitors in antirejection effects but also augment the nephrotoxicity of both cyclosporine and tacrolimus. They allow marked reduction in calcineurin inhibitor drug doses, which also reduces the nephrotoxicity of the combinations. In clinical trials in kidney, heart, lung, small bowel, pancreas, islet and liver transplantation in combination with cyclosporine and tacrolimus, rejection rates are equivalent or superior to those achieved with mycophenolate mofetil combinations. Despite this, its clinical usage remains limited. The side-effect profile, especially elevations in serum lipids and nephrotoxicity when administered in combination with calcineurin inhibitors, are the major factors. However, these drugs are finding an increasing place in other areas of medicine, including incorporation into endovascular coronary artery and peripheral arterial stents and in cancer therapy. Their ability to reduce fibrosis and neovascularization suggests other areas of potential use.
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2,333,164 |
Contributions of endothelium-derived relaxing factors to control of hindlimb blood flow in the mouse in vivo.
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We determined the contributions of various endothelium-derived relaxing factors to control of basal vascular tone and endothelium-dependent vasodilation in the mouse hindlimb in vivo. Under anesthesia, catheters were placed in a carotid artery, jugular vein, and femoral artery (for local hindlimb circulation injections). Hindlimb blood flow (HBF) was measured by transit-time ultrasound flowmetry. N(omega)-nitro-L-arginine methyl ester (L-NAME, 50 mg/kg plus 10 mg x kg(-1) x h(-1)), to block nitric oxide (NO) production, altered basal hemodynamics, increasing mean arterial pressure (30 +/- 3%) and reducing HBF (-30 +/- 12%). Basal hemodynamics were not significantly altered by indomethacin (10 mg x kg(-1) x h(-1)), charybdotoxin (ChTx, 3 x 10(-8) mol/l), apamin (2.5 x 10(-7) mol/l), or ChTx plus apamin (to block endothelium-derived hyperpolarizing factor; EDHF). Hyperemic responses to local injection of acetylcholine (2.4 microg/kg) were reproducible in vehicle-treated mice and were not significantly attenuated by L-NAME alone, indomethacin alone, L-NAME plus indomethacin with or without co-infusion of diethlyamine NONOate to restore resting NO levels, ChTx alone, or apamin alone. Hyperemic responses evoked by acetylcholine were reduced by 29 +/- 11% after combined treatment with apamin plus charybdotoxin, and the remainder was virtually abolished by additional treatment with L-NAME but not indomethacin. None of the treatments altered the hyperemic response to sodium nitroprusside (5 microg/kg). We conclude that endothelium-dependent vasodilation in the mouse hindlimb in vivo is mediated by both NO and EDHF. EDHF can fully compensate for the loss of NO, but this cannot be explained by tonic inhibition of EDHF by NO. Control of basal vasodilator tone in the mouse hindlimb is dominated by NO.
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2,333,165 |
Examining the influence of maternal bradycardia on neonatal outcome using automated data collection.
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Due to the increasing number of caesarean sections, we investigated the influence of maternal bradycardia during general and regional anaesthesia on seven standard paediatric outcome parameters using our online recorded data.</AbstractText>Data from 1154 women undergoing caesarean section were investigated prospectively. Bradycardia was defined as a heart rate below 60 beats/min. The matched-pairs method was used to evaluate the impact of bradycardia on Apgar scores at 1, 5, and 10 min, umbilical artery pH and base excess, admission to paediatric intensive care unit, and seven-day mortality. Matched references were automatically selected among all patients from the data pool according to anaesthetic technique, sensory block height, urgency, maternal age and body mass index. Stepwise regression models were developed to predict the impact of intra-operative bradycardia on outcome variables with differences between matched pairs assessed using univariate analysis.</AbstractText>Bradycardia was found in 146 women (12.7%) for whom a control could be matched in 131 cases (89.7%). Mean 5-minute Apgar score was 9.2+/-1.1 for study patients and 9.3+/-1.1 for controls. pH and base excess were not significantly different between groups. In cases of urgent surgery, neonates had an increased risk of 1.8 (95% CI 1.36-2.44, P<0.01) for an Apgar score <or= 8 at 1 min and a 2.6-fold risk (95% CI 1.64-4.06, P<0.01) of umbilical arterial pH of <or= 7.2 compared to infants undergoing non-urgent procedures.</AbstractText>Using matched-pairs analysis we were unable to demonstrate that episodes of maternal bradycardia below 60 beats/min were associated with a poorer neonatal outcome regardless of anaesthetic technique.</AbstractText>
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2,333,166 |
Epidural clonidine added to a bupivacaine infusion increases analgesic duration in labor without adverse maternal or fetal effects.
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Many obstetric patients receiving epidural analgesia are encouraged to ambulate. This current study was designed to determine the potential for maximizing the time to first epidural supplement when adding clonidine to a 0.625 mg.ml(-1) bupivacaine continuous epidural infusion following epidural fentanyl bolus in early labor for patients allowed to ambulate. Maternal and fetal effects secondary to clonidine were also evaluated.</AbstractText>Sixty-eight laboring primigravid women received a 3-ml epidural test dose of lidocaine with epinephrine, followed by a fentanyl 100-microg bolus (in a 10 ml-volume). The patients then received a 0.625 mg.ml(-1) bupivacaine continuous epidural infusion, either with or without clonidine (5 microg.ml(-1)), at a rate of 10 ml.h(-1). Pain scores and side effects were recorded for each patient.</AbstractText>The overall quality of analgesia was similar in both groups. The mean duration prior to request for additional analgesia was significantly longer in the clonidine group (269 +/- 160 min), compared to the control group (164 +/- 64 min). No patient in either group experienced any detectable motor block; one patient (clonidine group) complained of mild thigh numbness and was not allowed to ambulate. While mean blood pressure was approximately 6 mmHg lower in the clonidine group at 1, 1.5, and 3.5 h, this was not clinically significant. No adverse effects on maternal heart rate or fetal heart rate were noted.</AbstractText>In early laboring patients, addition of clonidine prolongs the analgesia duration of a 0.625 mg.ml(-1) bupivacaine continuous epidural infusion following 100 microg epidural fentanyl (after a lidocaine-epinephrine test dose) without a clinically significant increase in side effects.</AbstractText>
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2,333,167 |
Ultrasonographic guidance for sciatic and femoral nerve blocks in children.
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Recent studies have shown that ultrasound guidance for paediatric regional anaesthesia can improve the quality of upper extremity and neuraxial blocks. We therefore investigated whether ultrasound guidance for sciatic and femoral nerve blocks prolongs sensory blockade in comparison with nerve stimulator guidance in children.</AbstractText>Forty-six children scheduled for surgery of one lower extremity were randomized to receive a sciatic and femoral nerve block under either ultrasound or nerve stimulator guidance. After induction of general anaesthesia, the blocks were performed using an ultrasound-guided multiple injection technique until the nerves were surrounded by levobupivacaine, or by nerve stimulator guidance using a predefined dose of 0.3 ml kg(-1) of levobupivacaine. An increase in heart rate of more than 15% of baseline during surgery defined a failed block. The duration of the block was determined from the injection of local anaesthetic to the time when the patient received the first postoperative analgesic.</AbstractText>Two blocks in the nerve stimulator group failed. There were no failures in the ultrasound group. The duration of analgesia was longer in the ultrasound group mean (sd) 508 (178) vs 335 (169) min (P < 0.05). The volume of local anaesthetic in sciatic and femoral nerve blocks was reduced with ultrasound compared with nerve stimulator guidance [0.2 (0.06) vs 0.3 ml kg(-1) (P < 0.001) and 0.15 (0.04) vs 0.3 ml kg(-1) (P < 0.001), respectively].</AbstractText>Ultrasound guidance for sciatic and femoral nerve blocks in children increased the duration of sensory blockade in comparison with nerve stimulator guidance. Prolonged sensory blockade was achieved with smaller volumes of local anaesthetic when using ultrasound guidance.</AbstractText>
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2,333,168 |
Levobupivacaine-induced seizures and cardiovascular collapse treated with Intralipid.
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Lipid emulsion has been used in the successful treatment of local anaesthetic-induced cardiovascular collapse in animals and in two cases of cardiac arrest in humans. Previous reports of levobupivacaine toxicity in humans have been characterised by neurological signs and symptoms, without serious cardiovascular events. We present a case in which presumed intravenous injection of levobupivacaine led to neurological and cardiovascular consequences. This was treated successfully by resuscitation that included intravenous Intralipid infusion.
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2,333,169 |
Immunomodulation by maternal autoantibodies of the fetal serotoninergic 5-HT4 receptor and its consequences in early BALB/c mouse embryonic development.
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The presence of functional 5-HT4 receptors in human and its involvement in neonatal lupus erythematosus (NLE) have prompted us to study the receptor expression and role during embryogenesis. Earlier we managed to demonstrate that female BALB/c mice immunized against the second extracellular loop (SEL) of the 5-HT4 receptor gave birth to pups with heart block. To explain this phenomenon we investigated the expression of 5-HT4 receptors during mouse embryogenesis. At the same time we looked whether the consequence of 5-HT4 receptor immunomodulation observed earlier is in relation to receptor expression. We studied the expression of 5-HT4 receptor at the mRNA level and its two isoforms 5-HT4(a) and 5-HT4(d) at the protein level in embryos from BALB/c mice, at 8th, 12th, 18th gestation days (GD) and 1 day post natal (DPN). Simultaneously the receptor activity was inhibited by rising antibodies, in female mice against SEL of the receptor. The mice were mated and embryos were collected at 8th, 12th, 18th GD and 1 DPN.</AbstractText>5-HT4 receptor mRNA increased in brain from 12th GD to 1 DPN. Its expression gradually decreased in heart and disappeared at birth. This was consistent with expression of the receptor isoforms 5-HT4(a) and (d). Abnormalities like decreased number of embryos, growth delay, spina bifida and sinus arrhythmia from 12th GD were documented in pups of mice showing anti-5-HT4 receptor antibodies.</AbstractText>serotoninergic 5-HT4 receptor plays an important role in mouse foetal development. In BALB/c mice there is a direct relation between the expression of receptor and the deleterious effect of maternal anti-5-HT4 receptor autoantibodies in early embryogenesis.</AbstractText>
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2,333,170 |
Hypnosis prevents the cardiovascular response to cold pressor test.
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To highlight the effects of hypnotic focused analgesia (HFA), 20 healthy participants underwent a cold pressor test (CPT) in waking basal conditions (WBC) by keeping the right hand in icy water until tolerable (pain tolerance); subjective pain was quantified by visual scale immediately before extracting the hand from water. The test was then repeated while the participants were under hypnosis and underwent HFA suggestions. Cardiovascular parameters were continuously monitored. Pain tolerance was 121.5+/-96.1 sec in WBC and 411.0+/-186.7 sec during HFA (p < 0.0001), and visual rating score 7.75+/-2.29 and 2.45+/-2.98 (p < 0.0001), respectively. CPT-induced increase of total peripheral resistance was non significant during HFA and +21% (p < 0.01) in WBC. HFA therefore reduced both perception and the reflex cardiovascular consequences of pain as well. This indicates that hypnotic analgesia implies a decrease of sensitivity and/or a block of transmission of painful stimuli, with depression of the nervous reflex arc.
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2,333,171 |
Synthesis of murisolin, (15R, 16R, 19R, 20S)-murisolin A, and (15R, 16R, 19S, 20S)-16,19-cis-murisolin and their inhibitory action with bovine heart mitochondrial complex I.
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The asymmetric total synthesis of murisolin, (15R, 16R, 19R, 20S)-murisolin A, and (15R, 16R, 19S, 20S)-16,19-cis-murisolin was performed by using an epoxy alcohol as a versatile chiral building block for synthesizing the stereoisomers of mono-THF annonaceous acetogenins. The inhibitory activity of these murisolin compounds was examined with bovine heart mitochondrial complex I, and they showed almost the same activity.
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2,333,172 |
Mechanical efficiency and wheelchair performance during and after spinal cord injury rehabilitation.
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The purpose of the present study was to investigate whether mechanical efficiency (ME) relates to wheelchair propulsion capacity and wheelchair performance tasks during and after rehabilitation of people with a spinal cord injury (SCI). Eighty participants with a SCI were tested during rehabilitation (3 x) and 1 year after discharge. Two 3-minute submaximal exercise blocks, a maximal wheelchair exercise test, and four wheelchair performance tasks were performed. ME, peak power output (PO (peak)), the sum of the performance times of a 15-m sprint and figure-of-eight, and the heart rate reserve (%HRR) during 10 s of wheelchair propulsion on a 3 % and 6 % slope were calculated. The relationship between ME and PO (peak), %HRR and performance time was tested with a multilevel regression analysis. ME showed a significant relationship with PO (peak) (p </= 0.002). A 1 % higher ME related to a 1.6 - 2.2 W higher PO (peak). ME of exercise block 2 was related to the sum of the performance times of a 15-m sprint and figure-of-eight; the tests were performed faster by participants with a higher ME. No relationship was found between ME and %HRR during wheelchair propulsion on a slope. ME showed a significant effect on wheelchair propulsion capacity and wheelchair performance time during and 1 yr after SCI rehabilitation although the isolated effect of ME is small.
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2,333,173 |
Cross-sample entropy statistic as a measure of complexity and regularity of renal sympathetic nerve activity in the rat.
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In this study, we employed both power spectral analysis and cross-sample entropy measurement to assess the relationship between two time series, arterial blood pressure (ABP) and renal sympathetic nerve activity (RSNA), during a mild haemorrhage in anaesthetized Wistar rats. Removal of 1 ml of venous blood decreased BP (by 7.1 +/- 0.7 mmHg) and increased RSNA (by 25.9 +/- 2.4%). During these changes, the power in the RSNA signal at heart rate frequency was reduced but coherence between the spectra at heart rate frequency in RSNA and ABP remained unchanged. Cross-sample entropy was significantly increased (by 10%) by haemorrhage, revealing that there was greater asynchrony between ABP and the RSNA time series. Intrathecal administration of the glutamate receptor antagonist kynurenic acid (2 mm) almost halved (P < 0.01) the reflex increase in RSNA. Also during kynurenic acid block, haemorrhage failed to change total power, power at heart rate frequency, coherence at heart rate frequency, or the cross-sample entropy measurements. We conclude that the increase in asynchrony between ABP and RSNA during the reflex increase in RSNA was a consequence of an increase in synaptic input to the spinal renal neurones. The data show that the cross-sample entropy calculations can characterize the non-linearities of neural mechanisms underlying cardiovascular control and have a potential to reveal how some aspects of homeostatic regulation of kidney function is achieved by the autonomic nervous system.
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2,333,174 |
Quantification and MRI validation of regional contractile dysfunction in mice post myocardial infarction using high resolution ultrasound.<Pagination><StartPage>894</StartPage><EndPage>904</EndPage><MedlinePgn>894-904</MedlinePgn></Pagination><Abstract><AbstractText>A versatile, computationally efficient two-dimensional (2D) speckle-tracking method based on high resolution ultrasound imaging is proposed to quantify regional myocardial dysfunction in mice. Ultrasound scans were performed on the hearts of normal and post myocardial infarction (MI) mice with a Vevo770 scanner (VisualSonics, Toronto, Canada) operating at 30 MHz frequency. Regional myocardial motion was tracked using a 2D minimum sum of absolute differences (MSAD) block-matching algorithm. Motion analyses calculated from ultrasound images were compared with gold-standard analyses performed using small animal magnetic resonance imaging (MRI). The radial and circumferential components of strain were compared between ultrasound and MRI short axis views and promising correlations were obtained (r = 0.90 and r = 0.85 for radial and circumferential strain, respectively). Therefore, ultrasound imaging, followed by 2D image tracking, provides an effective, low cost, mobile method to quantify murine cardiac function accurately and reliably.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Yinbo</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Biomedical Engineering, University of Virginia, Charlottesville, VA 22908-0759, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Garson</LastName><ForeName>Christopher D</ForeName><Initials>CD</Initials></Author><Author ValidYN="Y"><LastName>Xu</LastName><ForeName>Yaqin</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Beyers</LastName><ForeName>Ronald J</ForeName><Initials>RJ</Initials></Author><Author ValidYN="Y"><LastName>Epstein</LastName><ForeName>Frederick H</ForeName><Initials>FH</Initials></Author><Author ValidYN="Y"><LastName>French</LastName><ForeName>Brent A</ForeName><Initials>BA</Initials></Author><Author ValidYN="Y"><LastName>Hossack</LastName><ForeName>John A</ForeName><Initials>JA</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>RR022582</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>HL058582</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 EB001826-01</GrantID><Acronym>EB</Acronym><Agency>NIBIB NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>S10 RR022582</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>S10 RR022582-01</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 EB001826</GrantID><Acronym>EB</Acronym><Agency>NIBIB NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>EB001826</GrantID><Acronym>EB</Acronym><Agency>NIBIB NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL058582</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2007</Year><Month>04</Month><Day>16</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Ultrasound Med Biol</MedlineTA><NlmUniqueID>0410553</NlmUniqueID><ISSNLinking>0301-5629</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000465" MajorTopicYN="N">Algorithms</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004452" MajorTopicYN="N">Echocardiography</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="Y">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006321" MajorTopicYN="N">Heart</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007091" MajorTopicYN="N">Image Processing, Computer-Assisted</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018810" MajorTopicYN="N">Magnetic Resonance Angiography</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009200" MajorTopicYN="N">Myocardial Contraction</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009203" MajorTopicYN="N">Myocardial Infarction</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="Y">diagnostic imaging</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011859" MajorTopicYN="N">Radiography</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013314" MajorTopicYN="N">Stress, Mechanical</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013997" MajorTopicYN="N">Time Factors</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2006</Year><Month>8</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2006</Year><Month>12</Month><Day>6</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2006</Year><Month>12</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2007</Year><Month>4</Month><Day>17</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2007</Year><Month>8</Month><Day>21</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2007</Year><Month>4</Month><Day>17</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">17434660</ArticleId><ArticleId IdType="mid">NIHMS25560</ArticleId><ArticleId IdType="pmc">PMC2136434</ArticleId><ArticleId IdType="doi">10.1016/j.ultrasmedbio.2006.12.008</ArticleId><ArticleId IdType="pii">S0301-5629(07)00011-7</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Aboagye EO. Positron emission tomography imaging of small animals in anticancer drug development. Mol Imaging Biol. 2005;7(1):53–8.</Citation><ArticleIdList><ArticleId IdType="pubmed">15912276</ArticleId></ArticleIdList></Reference><Reference><Citation>Acton PD, Kung HF. Small animal imaging with high resolution single photon emission tomography. Nucl Med Biol. 2003;30(8):889–95.</Citation><ArticleIdList><ArticleId IdType="pubmed">14698793</ArticleId></ArticleIdList></Reference><Reference><Citation>Amundsen B, Helle-Valle T, Edvardsen T, et al. Noninvasive myocardial strain measurement by speckle tracking echocardiography: validation against sonomicrometry and tagged magnetic resonance imaging. J Am Coll Cardiol. 2006;47:789–93.</Citation><ArticleIdList><ArticleId IdType="pubmed">16487846</ArticleId></ArticleIdList></Reference><Reference><Citation>Anderson T, Denvir M, Sharif I, et al. High frequency linear array scanner for the imaging of small rodents. IEEE Ultrasonics Symposium. 2003;2:1935– 1937.</Citation></Reference><Reference><Citation>Arai A, Gaither Cr, Epstein F, Balaban R, Wolff S. Myocardial velocity gradient imaging by phase contrast MRI with application to regional function in myocardial ischemia. Magn Reson Med. 1999;49(2):98–109.</Citation><ArticleIdList><ArticleId IdType="pubmed">10398955</ArticleId></ArticleIdList></Reference><Reference><Citation>Aristizabal O, Turnbull DH, Ketterling JA. Mouse embryo imaging with a 40-MHz annular array. IEEE Ultrasonics Symposium. 2005:361–364.</Citation></Reference><Reference><Citation>Bax JJ, Ansalone G, Breithardt OA, et al. Echocardiographic evaluation of cardiac resynchronization therapy: ready for routine clinical use?: A critical appraisal. J Am Coll Cardiol. 2004;44(1):1–9.</Citation><ArticleIdList><ArticleId IdType="pubmed">15234396</ArticleId></ArticleIdList></Reference><Reference><Citation>Bland JM, Altman DG. Statistical methods for assessing agreement between two methods of clinical measurement. Lancet. 1986;1(8476):307–10.</Citation><ArticleIdList><ArticleId IdType="pubmed">2868172</ArticleId></ArticleIdList></Reference><Reference><Citation>Breithardt O, Stellbrink C, Kramer A, et al. Echocardiographic quantification of left ventricular asynchrony predicts an acute hemodynamic benefit of cardiac resynchronization therapy. J Am Coll Cardiol. 2002;40(3):536–45.</Citation><ArticleIdList><ArticleId IdType="pubmed">12142123</ArticleId></ArticleIdList></Reference><Reference><Citation>Cerqueira MD, Weissman NJ, Dilsizian V, et al. Standardized myocardial segmentation and nomenclature for tomographic imaging of the heart: a statement for healthcare professionals from the Cardiac Imaging Committee of the Council on Clinical Cardiology of the American Heart Association. Circulation. 2002;105:539–542.</Citation><ArticleIdList><ArticleId IdType="pubmed">11815441</ArticleId></ArticleIdList></Reference><Reference><Citation>Cherin E, Williams R, Needles A, et al. Ultrahigh frame rate retrospective ultrasound microimaging and blood flow visualization in mice in vivo. Ultrasound Med Biol. 2006;32(5):683–91.</Citation><ArticleIdList><ArticleId IdType="pubmed">16677928</ArticleId></ArticleIdList></Reference><Reference><Citation>D'hooge J, Heimdal A, Jamal F, Sutherland G. Regional strain and strain rate measurements by cardiac ultrasound: Principles, implementation and limitations. Eur J Echocardiog. 2000;1(3):154–170.</Citation><ArticleIdList><ArticleId IdType="pubmed">11916589</ArticleId></ArticleIdList></Reference><Reference><Citation>D'hooge J, Thijs D, Sipido K, et al. Ultrasonic strain and strain rate imaging for the assessment of regional myocardial function in mice. IEEE Ultrasonics Symposium. 2004:470–473.</Citation></Reference><Reference><Citation>Dawson D, Lygate CA, Saunders J, et al. Quantitative 3-dimensional echocardiography for accurate and rapid cardiac phenotype characterization in mice. Circulation. 2004;110(12):1632–7.</Citation><ArticleIdList><ArticleId IdType="pubmed">15364813</ArticleId></ArticleIdList></Reference><Reference><Citation>Epstein FH, Yang Z, Gilson WD, et al. MR tagging early after myocardial infarction in mice demonstrates contractile dysfunction in adjacent and remote regions. Magn Reson Med. 2002;48(2):399–403.</Citation><ArticleIdList><ArticleId IdType="pubmed">12210951</ArticleId></ArticleIdList></Reference><Reference><Citation>Friemel BH, Bohs LN, Trahey GE. Relative performance of two-dimensional speckle-tracking techniques: normalized correlation, non-normalized correlation and sum absolute difference. IEEE Ultrasonics Symposium. 1995;2:1481–1484.</Citation></Reference><Reference><Citation>Gilson WD, Yang Z, French BA, Epstein FH. Complementary displacement-encoded MRI for contrast-enhanced infarct detection and quantification of myocardial function in mice. Magn Reson Med. 2004;51:744–752.</Citation><ArticleIdList><ArticleId IdType="pubmed">15065247</ArticleId></ArticleIdList></Reference><Reference><Citation>Gilson WD, Yang Z, French BA, Epstein FH. Measurement of myocardial mechanics in mice before and after infarction using multislice displacement-encoded MRI with 3D motion encoding. Am J Physiol Heart Circ Physiol. 2005;288:H1491–H1497.</Citation><ArticleIdList><ArticleId IdType="pubmed">15513963</ArticleId></ArticleIdList></Reference><Reference><Citation>Gleason S, Sari-Sarraf H, Paulus M, et al. Reconstruction of multi-energy X-Ray computer tomography images of laboratory mice. IEEE Trans Nucl Sci. 1999;46(4):1081–1086.</Citation></Reference><Reference><Citation>Heimdal A, Stoylen A, Torp H, Skjaerpe T. Real-time strain rate imaging of the left ventricle by ultrasound. J Am Soc Echocardiogr. 1998;11(11):1013–1019.</Citation><ArticleIdList><ArticleId IdType="pubmed">9812093</ArticleId></ArticleIdList></Reference><Reference><Citation>Kerry SM, Bland JM. Sample size in cluster randomisation. BMJ. 1998;316(7130):549.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC2665662</ArticleId><ArticleId IdType="pubmed">9501723</ArticleId></ArticleIdList></Reference><Reference><Citation>Killip S, Mahfoud Z, Pearce K. What is an intracluster correlation coefficient? Crucial concepts for primary care researchers. Ann Fam Med. 2004;2(3):204–8.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC1466680</ArticleId><ArticleId IdType="pubmed">15209195</ArticleId></ArticleIdList></Reference><Reference><Citation>Langeland S, D'hooge J, Wouters PF, et al. Experimental validation of a new ultrasound method for the simultaneous assessment of radial and longitudinal myocardial deformation independent of insonation angle. Circulation. 2005;112(14):2157–62.</Citation><ArticleIdList><ArticleId IdType="pubmed">16203928</ArticleId></ArticleIdList></Reference><Reference><Citation>Leitman M, Lysyansky P, Sidenko S, et al. Two-dimensional strain-a novel software for real-time quantitative echocardiographic assessment of myocardial function. J Am Soc Echocardiogr. 2004;17(10):1021–9.</Citation><ArticleIdList><ArticleId IdType="pubmed">15452466</ArticleId></ArticleIdList></Reference><Reference><Citation>Liu JH, Jeng GS, Wu TK, Li PC. ECG triggering and gating for ultrasonic small animal imaging. IEEE Trans Ultrason Ferroelectr Freq Control. 2006;53(9):1590–6.</Citation><ArticleIdList><ArticleId IdType="pubmed">16964909</ArticleId></ArticleIdList></Reference><Reference><Citation>Michael L, Entman M, Hartley C, et al. Myocardial ischemia and reperfusion: a murine model. Am J Physiol Heart Circ Physiol. 1995;269(6):H2147–H2154.</Citation><ArticleIdList><ArticleId IdType="pubmed">8594926</ArticleId></ArticleIdList></Reference><Reference><Citation>Moaveni S. Finite element analysis: theory and application with ANSYS. Upper Saddle River, NJ: Prentice Hall; 1999.</Citation></Reference><Reference><Citation>Scherrer-Crosbie M, Steudel W, Hunziker R, et al. Three-dimensional echocardiographic assessment of left ventricular wall motion abnormalities in mouse myocardial infarction. Journal of American Society of Echocardiography. 1999;12(10):834–840.</Citation><ArticleIdList><ArticleId IdType="pubmed">10511652</ArticleId></ArticleIdList></Reference><Reference><Citation>Sebag IA, Handschumacher MD, Ichinose F, et al. Quantitative assessment of regional myocardial function in mice by tissue Doppler imaging: comparison with hemodynamics and sonomicrometry. Circulation. 2005;111:2611–2616.</Citation><ArticleIdList><ArticleId IdType="pubmed">15897347</ArticleId></ArticleIdList></Reference><Reference><Citation>Shah D, Judd R, Kim R. Technology Insight: MRI of the myocardium. Nat Clin Pract Cardiovasc Med. 2005;2(11):597–605.</Citation><ArticleIdList><ArticleId IdType="pubmed">16258572</ArticleId></ArticleIdList></Reference><Reference><Citation>Streif J, Herold V, Szimtenings M, et al. In vivo time-resolved quantitative motion mapping of the murine myocardium with phase contrast MRI. Magn Reson Med. 2003;49(2):315–21.</Citation><ArticleIdList><ArticleId IdType="pubmed">12541252</ArticleId></ArticleIdList></Reference><Reference><Citation>Sutherland GR, Stewart MJ, Groundstroem KW, et al. Color Doppler myocardial imaging: a new technique for the assessment of myocardial function. J Am Soc Echocardiogr. 1994;7(5):441–458.</Citation><ArticleIdList><ArticleId IdType="pubmed">7986541</ArticleId></ArticleIdList></Reference><Reference><Citation>Toyoda T, Baba H, Akasaka T, et al. Assessment of regional myocardial strain by a novel automated tracking system from digital image files. J Am Soc Echocardiogr. 2004;17(12):1234–8.</Citation><ArticleIdList><ArticleId IdType="pubmed">15562260</ArticleId></ArticleIdList></Reference><Reference><Citation>Yang Z, Zingarelli B, Szabo C. The crucial role of endogenous interleukin-10 production in myocardial ischemia-reperfusion injury. Circulation. 2000;101:1019–1026.</Citation><ArticleIdList><ArticleId IdType="pubmed">10704170</ArticleId></ArticleIdList></Reference><Reference><Citation>Yang Z, Zingarelli B, Szabo C. Effect of genetic disruption of poly (ADP-ribose) synthetase on delayed production of inflammatory mediators and delayed necrosis during myocardial ischemia-reperfusion injury. Shock. 2000;13:60–66.</Citation><ArticleIdList><ArticleId IdType="pubmed">10638671</ArticleId></ArticleIdList></Reference><Reference><Citation>Yu Y, Acton S. Segmentation of ultrasound imagery using anisotropic diffusion. Proc 35th Asilomar Conf on Signals, Systems and Computers. 2001;2:1151–5.</Citation></Reference><Reference><Citation>Zerhouni E, Parish D, Rogers W, Yang A, Shapiro E. Human heart: tagging with MR imaging--a method for noninvasive assessment of myocardial motion. Radiology. 1988;169:59–63.</Citation><ArticleIdList><ArticleId IdType="pubmed">3420283</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">17433990</PMID><DateCompleted><Year>2007</Year><Month>09</Month><Day>26</Day></DateCompleted><DateRevised><Year>2007</Year><Month>04</Month><Day>16</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1092-9126</ISSN><JournalIssue CitedMedium="Print"><PubDate><Year>2007</Year></PubDate></JournalIssue><Title>Seminars in thoracic and cardiovascular surgery. Pediatric cardiac surgery annual</Title><ISOAbbreviation>Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu</ISOAbbreviation></Journal>Partial atrioventricular canal: pitfalls in technique.<Pagination><StartPage>42</StartPage><EndPage>46</EndPage><MedlinePgn>42-6</MedlinePgn></Pagination><Abstract><AbstractText>Partial atrioventricular (AV) canal represents approximately 25% of all AV septal defects. While often grouped with secundum ASD from the perspective of cardiopulmonary physiology, clinical presentation, and timing of surgical correction, their optimal management truly requires an understanding of their anatomic similarities to other forms of common AVC defects. By most measures, outcomes for surgical management of partial AV canal has improved over the last four decades, though some aspects of these defects continue to pose important challenges. Current experience has witnessed the reduction in early mortality and only rare complete heart block. Left AV valve dysfunction remains the most common indication for reoperation (10%) with LVOT stenosis the next most common reason (10% to 15% incidence, 5% to 10% reoperation rate). It is important to understand in this population that postoperative left AV valve problems and LVOT stenosis may be intimately linked, both from an etiologic standpoint, and with respect to their management.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Manning</LastName><ForeName>Peter B</ForeName><Initials>PB</Initials><AffiliationInfo><Affiliation>Division of Cardiothoracic Surgery, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA. [email protected]</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu</MedlineTA><NlmUniqueID>9815944</NlmUniqueID><ISSNLinking>1092-9126</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006348" MajorTopicYN="N">Cardiac Surgical Procedures</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="Y">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006325" MajorTopicYN="N">Heart Atria</DescriptorName><QualifierName UI="Q000002" MajorTopicYN="N">abnormalities</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006330" MajorTopicYN="N">Heart Defects, Congenital</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="Y">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006344" MajorTopicYN="N">Heart Septal Defects, Atrial</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006345" MajorTopicYN="N">Heart Septal Defects, Ventricular</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006349" MajorTopicYN="N">Heart Valve Diseases</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName><QualifierName UI="Q000002" MajorTopicYN="N">abnormalities</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011183" MajorTopicYN="N">Postoperative Complications</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012086" MajorTopicYN="N">Reoperation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014694" MajorTopicYN="N">Ventricular Outflow Obstruction</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>20</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2007</Year><Month>4</Month><Day>17</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2007</Year><Month>9</Month><Day>27</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2007</Year><Month>4</Month><Day>17</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">17433990</ArticleId><ArticleId IdType="doi">10.1053/j.pcsu.2007.02.002</ArticleId><ArticleId IdType="pii">S1092-9126(07)00024-5</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">17433986</PMID><DateCompleted><Year>2007</Year><Month>09</Month><Day>26</Day></DateCompleted><DateRevised><Year>2007</Year><Month>04</Month><Day>16</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1092-9126</ISSN><JournalIssue CitedMedium="Print"><PubDate><Year>2007</Year></PubDate></JournalIssue><Title>Seminars in thoracic and cardiovascular surgery. Pediatric cardiac surgery annual</Title><ISOAbbreviation>Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu</ISOAbbreviation></Journal>Atrioventricular canal: single-patch technique.<Pagination><StartPage>11</StartPage><EndPage>20</EndPage><MedlinePgn>11-20</MedlinePgn></Pagination><Abstract><AbstractText>Complete atrioventricular septal defects have been repaired at the Medical University of South Carolina for the past 25 years using the "single-patch technique" as first described by the Mayo Clinic group in 1968. In this technique, the single atrioventricular valve is separated into left (mitral) and right (tricuspid) components by dividing the superior and inferior bridging leaflets back to the annulus. A single patch of bovine pericardium is sutured to the right ventricular aspect of the ventricular septum, the previously divided valve leaflets are resuspended to the patch, the "cleft" in the left-sided valve is closed with interrupted sutures, and the atrial component of the defect closed by suturing the patch to the atrial septum with a continuous suture. Since 1995, there have been no operative deaths in the 88 consecutive infants undergoing this repair in our institution. Nine patients (10.2%) have required reoperation for severe mitral regurgitation. While the issue of operative mortality in patients undergoing single-patch repair of complete atrioventricular septal defect has largely been eliminated, residual or recurrent mitral regurgitation continues to be a problem.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Crawford</LastName><ForeName>Fred A</ForeName><Initials>FA</Initials><AffiliationInfo><Affiliation>Department of Surgery, Medical University of South Carolina, Charleston, SC 29425, USA. [email protected]</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu</MedlineTA><NlmUniqueID>9815944</NlmUniqueID><ISSNLinking>1092-9126</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D001022" MajorTopicYN="N">Aortic Valve Insufficiency</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006348" MajorTopicYN="N">Cardiac Surgical Procedures</DescriptorName><QualifierName UI="Q000295" MajorTopicYN="N">instrumentation</QualifierName><QualifierName UI="Q000379" MajorTopicYN="Y">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002315" MajorTopicYN="N">Cardiopulmonary Bypass</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004867" MajorTopicYN="N">Equipment Design</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006327" MajorTopicYN="N">Heart Block</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006344" MajorTopicYN="N">Heart Septal Defects, Atrial</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000601" MajorTopicYN="Y">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006345" MajorTopicYN="N">Heart Septal Defects, Ventricular</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000601" MajorTopicYN="Y">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007223" MajorTopicYN="N">Infant</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008944" MajorTopicYN="N">Mitral Valve Insufficiency</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010138" MajorTopicYN="N">Pacemaker, Artificial</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011183" MajorTopicYN="N">Postoperative Complications</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012086" MajorTopicYN="N">Reoperation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013022" MajorTopicYN="N" Type="Geographic">South Carolina</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016019" MajorTopicYN="N">Survival Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013536" MajorTopicYN="N">Suture Techniques</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014694" MajorTopicYN="N">Ventricular Outflow Obstruction</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2007</Year><Month>4</Month><Day>17</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2007</Year><Month>9</Month><Day>27</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2007</Year><Month>4</Month><Day>17</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">17433986</ArticleId><ArticleId IdType="doi">10.1053/j.pcsu.2007.01.017</ArticleId><ArticleId IdType="pii">S1092-9126(07)00018-X</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">17433985</PMID><DateCompleted><Year>2007</Year><Month>09</Month><Day>26</Day></DateCompleted><DateRevised><Year>2018</Year><Month>12</Month><Day>01</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1092-9126</ISSN><JournalIssue CitedMedium="Print"><PubDate><Year>2007</Year></PubDate></JournalIssue><Title>Seminars in thoracic and cardiovascular surgery. Pediatric cardiac surgery annual</Title><ISOAbbreviation>Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu</ISOAbbreviation></Journal>Overview: history, anatomy, timing, and results of complete atrioventricular canal.
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A versatile, computationally efficient two-dimensional (2D) speckle-tracking method based on high resolution ultrasound imaging is proposed to quantify regional myocardial dysfunction in mice. Ultrasound scans were performed on the hearts of normal and post myocardial infarction (MI) mice with a Vevo770 scanner (VisualSonics, Toronto, Canada) operating at 30 MHz frequency. Regional myocardial motion was tracked using a 2D minimum sum of absolute differences (MSAD) block-matching algorithm. Motion analyses calculated from ultrasound images were compared with gold-standard analyses performed using small animal magnetic resonance imaging (MRI). The radial and circumferential components of strain were compared between ultrasound and MRI short axis views and promising correlations were obtained (r = 0.90 and r = 0.85 for radial and circumferential strain, respectively). Therefore, ultrasound imaging, followed by 2D image tracking, provides an effective, low cost, mobile method to quantify murine cardiac function accurately and reliably.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Yinbo</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Biomedical Engineering, University of Virginia, Charlottesville, VA 22908-0759, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Garson</LastName><ForeName>Christopher D</ForeName><Initials>CD</Initials></Author><Author ValidYN="Y"><LastName>Xu</LastName><ForeName>Yaqin</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Beyers</LastName><ForeName>Ronald J</ForeName><Initials>RJ</Initials></Author><Author ValidYN="Y"><LastName>Epstein</LastName><ForeName>Frederick H</ForeName><Initials>FH</Initials></Author><Author ValidYN="Y"><LastName>French</LastName><ForeName>Brent A</ForeName><Initials>BA</Initials></Author><Author ValidYN="Y"><LastName>Hossack</LastName><ForeName>John A</ForeName><Initials>JA</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>RR022582</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>HL058582</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 EB001826-01</GrantID><Acronym>EB</Acronym><Agency>NIBIB NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>S10 RR022582</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>S10 RR022582-01</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 EB001826</GrantID><Acronym>EB</Acronym><Agency>NIBIB NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>EB001826</GrantID><Acronym>EB</Acronym><Agency>NIBIB NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL058582</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2007</Year><Month>04</Month><Day>16</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Ultrasound Med Biol</MedlineTA><NlmUniqueID>0410553</NlmUniqueID><ISSNLinking>0301-5629</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000465" MajorTopicYN="N">Algorithms</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004452" MajorTopicYN="N">Echocardiography</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="Y">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006321" MajorTopicYN="N">Heart</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007091" MajorTopicYN="N">Image Processing, Computer-Assisted</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018810" MajorTopicYN="N">Magnetic Resonance Angiography</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009200" MajorTopicYN="N">Myocardial Contraction</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009203" MajorTopicYN="N">Myocardial Infarction</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="Y">diagnostic imaging</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011859" MajorTopicYN="N">Radiography</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013314" MajorTopicYN="N">Stress, Mechanical</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013997" MajorTopicYN="N">Time Factors</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2006</Year><Month>8</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2006</Year><Month>12</Month><Day>6</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2006</Year><Month>12</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2007</Year><Month>4</Month><Day>17</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2007</Year><Month>8</Month><Day>21</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2007</Year><Month>4</Month><Day>17</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">17434660</ArticleId><ArticleId IdType="mid">NIHMS25560</ArticleId><ArticleId IdType="pmc">PMC2136434</ArticleId><ArticleId IdType="doi">10.1016/j.ultrasmedbio.2006.12.008</ArticleId><ArticleId IdType="pii">S0301-5629(07)00011-7</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Aboagye EO. Positron emission tomography imaging of small animals in anticancer drug development. Mol Imaging Biol. 2005;7(1):53–8.</Citation><ArticleIdList><ArticleId IdType="pubmed">15912276</ArticleId></ArticleIdList></Reference><Reference><Citation>Acton PD, Kung HF. Small animal imaging with high resolution single photon emission tomography. Nucl Med Biol. 2003;30(8):889–95.</Citation><ArticleIdList><ArticleId IdType="pubmed">14698793</ArticleId></ArticleIdList></Reference><Reference><Citation>Amundsen B, Helle-Valle T, Edvardsen T, et al. Noninvasive myocardial strain measurement by speckle tracking echocardiography: validation against sonomicrometry and tagged magnetic resonance imaging. J Am Coll Cardiol. 2006;47:789–93.</Citation><ArticleIdList><ArticleId IdType="pubmed">16487846</ArticleId></ArticleIdList></Reference><Reference><Citation>Anderson T, Denvir M, Sharif I, et al. High frequency linear array scanner for the imaging of small rodents. IEEE Ultrasonics Symposium. 2003;2:1935– 1937.</Citation></Reference><Reference><Citation>Arai A, Gaither Cr, Epstein F, Balaban R, Wolff S. Myocardial velocity gradient imaging by phase contrast MRI with application to regional function in myocardial ischemia. Magn Reson Med. 1999;49(2):98–109.</Citation><ArticleIdList><ArticleId IdType="pubmed">10398955</ArticleId></ArticleIdList></Reference><Reference><Citation>Aristizabal O, Turnbull DH, Ketterling JA. Mouse embryo imaging with a 40-MHz annular array. IEEE Ultrasonics Symposium. 2005:361–364.</Citation></Reference><Reference><Citation>Bax JJ, Ansalone G, Breithardt OA, et al. Echocardiographic evaluation of cardiac resynchronization therapy: ready for routine clinical use?: A critical appraisal. J Am Coll Cardiol. 2004;44(1):1–9.</Citation><ArticleIdList><ArticleId IdType="pubmed">15234396</ArticleId></ArticleIdList></Reference><Reference><Citation>Bland JM, Altman DG. Statistical methods for assessing agreement between two methods of clinical measurement. Lancet. 1986;1(8476):307–10.</Citation><ArticleIdList><ArticleId IdType="pubmed">2868172</ArticleId></ArticleIdList></Reference><Reference><Citation>Breithardt O, Stellbrink C, Kramer A, et al. Echocardiographic quantification of left ventricular asynchrony predicts an acute hemodynamic benefit of cardiac resynchronization therapy. J Am Coll Cardiol. 2002;40(3):536–45.</Citation><ArticleIdList><ArticleId IdType="pubmed">12142123</ArticleId></ArticleIdList></Reference><Reference><Citation>Cerqueira MD, Weissman NJ, Dilsizian V, et al. Standardized myocardial segmentation and nomenclature for tomographic imaging of the heart: a statement for healthcare professionals from the Cardiac Imaging Committee of the Council on Clinical Cardiology of the American Heart Association. Circulation. 2002;105:539–542.</Citation><ArticleIdList><ArticleId IdType="pubmed">11815441</ArticleId></ArticleIdList></Reference><Reference><Citation>Cherin E, Williams R, Needles A, et al. Ultrahigh frame rate retrospective ultrasound microimaging and blood flow visualization in mice in vivo. Ultrasound Med Biol. 2006;32(5):683–91.</Citation><ArticleIdList><ArticleId IdType="pubmed">16677928</ArticleId></ArticleIdList></Reference><Reference><Citation>D'hooge J, Heimdal A, Jamal F, Sutherland G. Regional strain and strain rate measurements by cardiac ultrasound: Principles, implementation and limitations. Eur J Echocardiog. 2000;1(3):154–170.</Citation><ArticleIdList><ArticleId IdType="pubmed">11916589</ArticleId></ArticleIdList></Reference><Reference><Citation>D'hooge J, Thijs D, Sipido K, et al. Ultrasonic strain and strain rate imaging for the assessment of regional myocardial function in mice. IEEE Ultrasonics Symposium. 2004:470–473.</Citation></Reference><Reference><Citation>Dawson D, Lygate CA, Saunders J, et al. Quantitative 3-dimensional echocardiography for accurate and rapid cardiac phenotype characterization in mice. Circulation. 2004;110(12):1632–7.</Citation><ArticleIdList><ArticleId IdType="pubmed">15364813</ArticleId></ArticleIdList></Reference><Reference><Citation>Epstein FH, Yang Z, Gilson WD, et al. MR tagging early after myocardial infarction in mice demonstrates contractile dysfunction in adjacent and remote regions. Magn Reson Med. 2002;48(2):399–403.</Citation><ArticleIdList><ArticleId IdType="pubmed">12210951</ArticleId></ArticleIdList></Reference><Reference><Citation>Friemel BH, Bohs LN, Trahey GE. Relative performance of two-dimensional speckle-tracking techniques: normalized correlation, non-normalized correlation and sum absolute difference. IEEE Ultrasonics Symposium. 1995;2:1481–1484.</Citation></Reference><Reference><Citation>Gilson WD, Yang Z, French BA, Epstein FH. Complementary displacement-encoded MRI for contrast-enhanced infarct detection and quantification of myocardial function in mice. Magn Reson Med. 2004;51:744–752.</Citation><ArticleIdList><ArticleId IdType="pubmed">15065247</ArticleId></ArticleIdList></Reference><Reference><Citation>Gilson WD, Yang Z, French BA, Epstein FH. Measurement of myocardial mechanics in mice before and after infarction using multislice displacement-encoded MRI with 3D motion encoding. Am J Physiol Heart Circ Physiol. 2005;288:H1491–H1497.</Citation><ArticleIdList><ArticleId IdType="pubmed">15513963</ArticleId></ArticleIdList></Reference><Reference><Citation>Gleason S, Sari-Sarraf H, Paulus M, et al. Reconstruction of multi-energy X-Ray computer tomography images of laboratory mice. IEEE Trans Nucl Sci. 1999;46(4):1081–1086.</Citation></Reference><Reference><Citation>Heimdal A, Stoylen A, Torp H, Skjaerpe T. Real-time strain rate imaging of the left ventricle by ultrasound. J Am Soc Echocardiogr. 1998;11(11):1013–1019.</Citation><ArticleIdList><ArticleId IdType="pubmed">9812093</ArticleId></ArticleIdList></Reference><Reference><Citation>Kerry SM, Bland JM. Sample size in cluster randomisation. BMJ. 1998;316(7130):549.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC2665662</ArticleId><ArticleId IdType="pubmed">9501723</ArticleId></ArticleIdList></Reference><Reference><Citation>Killip S, Mahfoud Z, Pearce K. What is an intracluster correlation coefficient? Crucial concepts for primary care researchers. Ann Fam Med. 2004;2(3):204–8.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC1466680</ArticleId><ArticleId IdType="pubmed">15209195</ArticleId></ArticleIdList></Reference><Reference><Citation>Langeland S, D'hooge J, Wouters PF, et al. Experimental validation of a new ultrasound method for the simultaneous assessment of radial and longitudinal myocardial deformation independent of insonation angle. Circulation. 2005;112(14):2157–62.</Citation><ArticleIdList><ArticleId IdType="pubmed">16203928</ArticleId></ArticleIdList></Reference><Reference><Citation>Leitman M, Lysyansky P, Sidenko S, et al. Two-dimensional strain-a novel software for real-time quantitative echocardiographic assessment of myocardial function. J Am Soc Echocardiogr. 2004;17(10):1021–9.</Citation><ArticleIdList><ArticleId IdType="pubmed">15452466</ArticleId></ArticleIdList></Reference><Reference><Citation>Liu JH, Jeng GS, Wu TK, Li PC. ECG triggering and gating for ultrasonic small animal imaging. IEEE Trans Ultrason Ferroelectr Freq Control. 2006;53(9):1590–6.</Citation><ArticleIdList><ArticleId IdType="pubmed">16964909</ArticleId></ArticleIdList></Reference><Reference><Citation>Michael L, Entman M, Hartley C, et al. Myocardial ischemia and reperfusion: a murine model. Am J Physiol Heart Circ Physiol. 1995;269(6):H2147–H2154.</Citation><ArticleIdList><ArticleId IdType="pubmed">8594926</ArticleId></ArticleIdList></Reference><Reference><Citation>Moaveni S. Finite element analysis: theory and application with ANSYS. Upper Saddle River, NJ: Prentice Hall; 1999.</Citation></Reference><Reference><Citation>Scherrer-Crosbie M, Steudel W, Hunziker R, et al. Three-dimensional echocardiographic assessment of left ventricular wall motion abnormalities in mouse myocardial infarction. Journal of American Society of Echocardiography. 1999;12(10):834–840.</Citation><ArticleIdList><ArticleId IdType="pubmed">10511652</ArticleId></ArticleIdList></Reference><Reference><Citation>Sebag IA, Handschumacher MD, Ichinose F, et al. Quantitative assessment of regional myocardial function in mice by tissue Doppler imaging: comparison with hemodynamics and sonomicrometry. Circulation. 2005;111:2611–2616.</Citation><ArticleIdList><ArticleId IdType="pubmed">15897347</ArticleId></ArticleIdList></Reference><Reference><Citation>Shah D, Judd R, Kim R. Technology Insight: MRI of the myocardium. Nat Clin Pract Cardiovasc Med. 2005;2(11):597–605.</Citation><ArticleIdList><ArticleId IdType="pubmed">16258572</ArticleId></ArticleIdList></Reference><Reference><Citation>Streif J, Herold V, Szimtenings M, et al. In vivo time-resolved quantitative motion mapping of the murine myocardium with phase contrast MRI. Magn Reson Med. 2003;49(2):315–21.</Citation><ArticleIdList><ArticleId IdType="pubmed">12541252</ArticleId></ArticleIdList></Reference><Reference><Citation>Sutherland GR, Stewart MJ, Groundstroem KW, et al. Color Doppler myocardial imaging: a new technique for the assessment of myocardial function. J Am Soc Echocardiogr. 1994;7(5):441–458.</Citation><ArticleIdList><ArticleId IdType="pubmed">7986541</ArticleId></ArticleIdList></Reference><Reference><Citation>Toyoda T, Baba H, Akasaka T, et al. Assessment of regional myocardial strain by a novel automated tracking system from digital image files. J Am Soc Echocardiogr. 2004;17(12):1234–8.</Citation><ArticleIdList><ArticleId IdType="pubmed">15562260</ArticleId></ArticleIdList></Reference><Reference><Citation>Yang Z, Zingarelli B, Szabo C. The crucial role of endogenous interleukin-10 production in myocardial ischemia-reperfusion injury. Circulation. 2000;101:1019–1026.</Citation><ArticleIdList><ArticleId IdType="pubmed">10704170</ArticleId></ArticleIdList></Reference><Reference><Citation>Yang Z, Zingarelli B, Szabo C. Effect of genetic disruption of poly (ADP-ribose) synthetase on delayed production of inflammatory mediators and delayed necrosis during myocardial ischemia-reperfusion injury. Shock. 2000;13:60–66.</Citation><ArticleIdList><ArticleId IdType="pubmed">10638671</ArticleId></ArticleIdList></Reference><Reference><Citation>Yu Y, Acton S. Segmentation of ultrasound imagery using anisotropic diffusion. Proc 35th Asilomar Conf on Signals, Systems and Computers. 2001;2:1151–5.</Citation></Reference><Reference><Citation>Zerhouni E, Parish D, Rogers W, Yang A, Shapiro E. Human heart: tagging with MR imaging--a method for noninvasive assessment of myocardial motion. Radiology. 1988;169:59–63.</Citation><ArticleIdList><ArticleId IdType="pubmed">3420283</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">17433990</PMID><DateCompleted><Year>2007</Year><Month>09</Month><Day>26</Day></DateCompleted><DateRevised><Year>2007</Year><Month>04</Month><Day>16</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1092-9126</ISSN><JournalIssue CitedMedium="Print"><PubDate><Year>2007</Year></PubDate></JournalIssue><Title>Seminars in thoracic and cardiovascular surgery. Pediatric cardiac surgery annual</Title><ISOAbbreviation>Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu</ISOAbbreviation></Journal><ArticleTitle>Partial atrioventricular canal: pitfalls in technique.</ArticleTitle><Pagination><StartPage>42</StartPage><EndPage>46</EndPage><MedlinePgn>42-6</MedlinePgn></Pagination><Abstract>Partial atrioventricular (AV) canal represents approximately 25% of all AV septal defects. While often grouped with secundum ASD from the perspective of cardiopulmonary physiology, clinical presentation, and timing of surgical correction, their optimal management truly requires an understanding of their anatomic similarities to other forms of common AVC defects. By most measures, outcomes for surgical management of partial AV canal has improved over the last four decades, though some aspects of these defects continue to pose important challenges. Current experience has witnessed the reduction in early mortality and only rare complete heart block. Left AV valve dysfunction remains the most common indication for reoperation (10%) with LVOT stenosis the next most common reason (10% to 15% incidence, 5% to 10% reoperation rate). It is important to understand in this population that postoperative left AV valve problems and LVOT stenosis may be intimately linked, both from an etiologic standpoint, and with respect to their management.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Manning</LastName><ForeName>Peter B</ForeName><Initials>PB</Initials><AffiliationInfo><Affiliation>Division of Cardiothoracic Surgery, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA. [email protected]</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu</MedlineTA><NlmUniqueID>9815944</NlmUniqueID><ISSNLinking>1092-9126</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006348" MajorTopicYN="N">Cardiac Surgical Procedures</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="Y">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006325" MajorTopicYN="N">Heart Atria</DescriptorName><QualifierName UI="Q000002" MajorTopicYN="N">abnormalities</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006330" MajorTopicYN="N">Heart Defects, Congenital</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="Y">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006344" MajorTopicYN="N">Heart Septal Defects, Atrial</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006345" MajorTopicYN="N">Heart Septal Defects, Ventricular</DescriptorName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006349" MajorTopicYN="N">Heart Valve Diseases</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName><QualifierName UI="Q000002" MajorTopicYN="N">abnormalities</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011183" MajorTopicYN="N">Postoperative Complications</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012086" MajorTopicYN="N">Reoperation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014694" MajorTopicYN="N">Ventricular Outflow Obstruction</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>20</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2007</Year><Month>4</Month><Day>17</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2007</Year><Month>9</Month><Day>27</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2007</Year><Month>4</Month><Day>17</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">17433990</ArticleId><ArticleId IdType="doi">10.1053/j.pcsu.2007.02.002</ArticleId><ArticleId IdType="pii">S1092-9126(07)00024-5</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">17433986</PMID><DateCompleted><Year>2007</Year><Month>09</Month><Day>26</Day></DateCompleted><DateRevised><Year>2007</Year><Month>04</Month><Day>16</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1092-9126</ISSN><JournalIssue CitedMedium="Print"><PubDate><Year>2007</Year></PubDate></JournalIssue><Title>Seminars in thoracic and cardiovascular surgery. Pediatric cardiac surgery annual</Title><ISOAbbreviation>Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu</ISOAbbreviation></Journal><ArticleTitle>Atrioventricular canal: single-patch technique.</ArticleTitle><Pagination><StartPage>11</StartPage><EndPage>20</EndPage><MedlinePgn>11-20</MedlinePgn></Pagination><Abstract>Complete atrioventricular septal defects have been repaired at the Medical University of South Carolina for the past 25 years using the "single-patch technique" as first described by the Mayo Clinic group in 1968. In this technique, the single atrioventricular valve is separated into left (mitral) and right (tricuspid) components by dividing the superior and inferior bridging leaflets back to the annulus. A single patch of bovine pericardium is sutured to the right ventricular aspect of the ventricular septum, the previously divided valve leaflets are resuspended to the patch, the "cleft" in the left-sided valve is closed with interrupted sutures, and the atrial component of the defect closed by suturing the patch to the atrial septum with a continuous suture. Since 1995, there have been no operative deaths in the 88 consecutive infants undergoing this repair in our institution. Nine patients (10.2%) have required reoperation for severe mitral regurgitation. While the issue of operative mortality in patients undergoing single-patch repair of complete atrioventricular septal defect has largely been eliminated, residual or recurrent mitral regurgitation continues to be a problem.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Crawford</LastName><ForeName>Fred A</ForeName><Initials>FA</Initials><AffiliationInfo><Affiliation>Department of Surgery, Medical University of South Carolina, Charleston, SC 29425, USA. [email protected]</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu</MedlineTA><NlmUniqueID>9815944</NlmUniqueID><ISSNLinking>1092-9126</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D001022" MajorTopicYN="N">Aortic Valve Insufficiency</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006348" MajorTopicYN="N">Cardiac Surgical Procedures</DescriptorName><QualifierName UI="Q000295" MajorTopicYN="N">instrumentation</QualifierName><QualifierName UI="Q000379" MajorTopicYN="Y">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002315" MajorTopicYN="N">Cardiopulmonary Bypass</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004867" MajorTopicYN="N">Equipment Design</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006327" MajorTopicYN="N">Heart Block</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006344" MajorTopicYN="N">Heart Septal Defects, Atrial</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000601" MajorTopicYN="Y">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006345" MajorTopicYN="N">Heart Septal Defects, Ventricular</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000601" MajorTopicYN="Y">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007223" MajorTopicYN="N">Infant</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008944" MajorTopicYN="N">Mitral Valve Insufficiency</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010138" MajorTopicYN="N">Pacemaker, Artificial</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011183" MajorTopicYN="N">Postoperative Complications</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012086" MajorTopicYN="N">Reoperation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013022" MajorTopicYN="N" Type="Geographic">South Carolina</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016019" MajorTopicYN="N">Survival Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013536" MajorTopicYN="N">Suture Techniques</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014694" MajorTopicYN="N">Ventricular Outflow Obstruction</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2007</Year><Month>4</Month><Day>17</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2007</Year><Month>9</Month><Day>27</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2007</Year><Month>4</Month><Day>17</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">17433986</ArticleId><ArticleId IdType="doi">10.1053/j.pcsu.2007.01.017</ArticleId><ArticleId IdType="pii">S1092-9126(07)00018-X</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">17433985</PMID><DateCompleted><Year>2007</Year><Month>09</Month><Day>26</Day></DateCompleted><DateRevised><Year>2018</Year><Month>12</Month><Day>01</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1092-9126</ISSN><JournalIssue CitedMedium="Print"><PubDate><Year>2007</Year></PubDate></JournalIssue><Title>Seminars in thoracic and cardiovascular surgery. Pediatric cardiac surgery annual</Title><ISOAbbreviation>Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu</ISOAbbreviation></Journal><ArticleTitle>Overview: history, anatomy, timing, and results of complete atrioventricular canal.</ArticleTitle><Pagination><StartPage>3</StartPage><EndPage>10</EndPage><MedlinePgn>3-10</MedlinePgn></Pagination><Abstract>The past 50 years have been marked by major advances in the care of children with complete atrioventricular canal defects. There have been important contributions from surgeons, cardiologists, and pathologists to provide us with our current understanding of the anatomy of atrioventricular canal defects and excellent surgical outcomes. In this monograph we will discuss the surgical contributions of Lillehei, Kirklin, McGoon, Maloney, Trusler, Wilcox, and Nunn. The improvements in outcomes achieved by these surgeons were made possible by the pathology and anatomy clarifications provided by Lev, Rastelli, and Anderson.
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2,333,175 |
Tramadol does not prolong the effect of ropivacaine 7.5 mg/ml for axillary brachial plexus block.
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The aim of this prospective, randomized, double-blind study was to evaluate the effect of the addition of tramadol to ropivacaine on the onset and duration of sensory and motor block, and duration of analgesia, for axillary brachial plexus block.</AbstractText>After institutional approval and informed consent had been obtained, 45 patients scheduled for forearm or hand surgery under axillary brachial plexus block were randomly allocated into two groups. The ropivacaine group received 40 ml of ropivacaine 7.5 mg/ml plus 2 ml of isotonic sodium chloride solution, and the tramadol group received 40 ml of ropivacaine 7.5 mg/ml plus 2 ml (100 mg) of tramadol. The onset and duration of sensory and motor block in the distribution of the musculocutaneous, radial, median and ulnar nerves, the duration of analgesia, the time to first pain medication, hemodynamics and side-effects were recorded.</AbstractText>The addition of tramadol did not improve the speed of onset or increase the duration of sensory and motor block. The durations of analgesia were 631 +/- 33 min and 633 +/- 37 min (mean +/- standard deviation) in the ropivacaine and tramadol groups, respectively (P > 0.05). Hemodynamic parameters and side-effects did not differ between the groups.</AbstractText>The addition of 100 mg of tramadol to 7.5 mg/ml of ropivacaine, for axillary brachial plexus block, does not prolong the duration of motor and sensory block and analgesia.</AbstractText>
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2,333,176 |
Update of diuretics in the treatment of hypertension.
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Diuretics, which are primarily used to modify the volume and the composition of body fluids, are widely used to treat hypertension. The diuretics include a) the thiazides and thiazide-like agents, which are the most common drugs used to treat high blood pressure (these drugs inhibit sodium reabsorption in the early distal convoluted tubule); b) loop diuretics, such as furosemide, block chloride and sodium reabsorption by inhibition of the Na/K/2Cl cotransport system in the thick ascending limb of the loop of Henle; and c) potassium-sparing (retaining) diuretics, including aldosterone receptor blockers (such as spironolactone and eplerenone) and epithelial sodium channel blockers (such as amiloride and triamterene, which interfere with the reabsorption of sodium and excretion of potassium and hydrogen that takes place in the late distal tubule, the connecting tubule, and the cortical collecting duct). Hydrochlorothiazide 12.5 mg once daily or equivalent low dosages of other similar agents reduce blood pressure in approximately one-half to two-thirds of patients who are responsive to this class of drugs; higher doses add little to the effect on blood pressure and also increase side effects. Some combinations of very small doses of thiazide diuretics - for example, 6.25 mg hydrochlorothiazide or 0.625 mg indapamide, with a low dose of an antihypertensive drug of a different class - have average antihypertensive efficacy when used once daily. Furosemide is used in patients with renal failure or severe heart failure and is best given by continuous intravenous infusion. The potassium-sparing diuretics are generally used in combination with thiazide diuretics to treat hypertension. Side effects occur at about the same frequency and severity with equipotent doses of all diuretics. The incidence of side effects is dose-dependent and also increases as a function of the duration of the renal excretory and antihypertensive actions. However, longer-acting diuretics provide better 24-hour control of blood pressure and increase compliance and adherence to the treatment regimen.
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2,333,177 |
Limited Wegener's granulomatosis--is it limited?
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Complete heart block associated with Wegener's granulomatosis (WG) is rare especially in the limited form of the disease. We describe a case of a 43-year-old woman with a limited form of WG who developed a complete heart block. Prompt treatment with steroids and cyclophosphamide led to temporary regression of complete heart block. Further involvement of lung was treated successfully by tumor necrosis factor-alpha inhibitor infliximab. Cardiac rhythm abnormalities should always be kept in mind both in diagnosis and follow-up of WG.
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2,333,178 |
An analysis of the effects of stretch on IGF-I secretion from rat ventricular fibroblasts.
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Mechanical force can induce a number of fundamental short- and long-term responses in myocardium. These include alterations in ECM, activation of cell-signaling pathways, altered gene regulation, changes in cell proliferation and growth, and secretion of a number of peptides and growth factors. It is now known that a number of these autocrine/paracrine factors are secreted from both cardiomyocytes and ventricular cardiac fibroblasts (CFb) in response to stretch. One such substance is IGF-I. IGF-I is an important autocrine/paracrine factor that can regulate physiological or pathophysiological responses, such as hypertrophy. In this study, we addressed the possible effects of mechanical perturbation, biaxial strain, on IGF-I secretion from adult rat CFb. CFb were subjected to either static stretch (3-10%) or cyclic stretch (10%; 0.1-1 Hz) over a 24-h period. IGF-1 secretion from CFb in response to selected stretch paradigms was examined using ELISA to measure IGF-I concentrations in conditioned media. Static stretch did not result in any measurable modulation of IGF-I secretion from CFb. However, cyclic stretch significantly increased IGF-I secretion from CFb in a frequency- and time-dependent manner compared with nonstretched controls. This stretch-induced increase in secretion was relatively insensitive to changes in extracellular [Ca(2+)] or to block of L-type Ca(2+) channels. In contrast, thapsigargin, an inhibitor of sarco(endo)plasmic reticulum Ca(2+) ATPase, remarkably decreased stretch-induced IGF-I secretion from CFb. We further show that IGF-I can upregulate mRNA expression of atrial natriuretic peptide in myocytes. In summary, cyclic stretch can significantly increase IGF-I secretion from CFb, and this effect is dependent on a thapsigargin-sensitive pool of intracellular [Ca(2+)].
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2,333,179 |
Differences in heart rate variability during haemodialysis and haemofiltration.
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The aim of our study was to evaluate whether convective (haemofiltration, Hf) and diffusive (haemodialysis, Hd) dialysis techniques induce different patterns of long- and short-term autonomic adjustments in haemodynamically stable dialysis patients.</AbstractText>Ten haemodynamically stable Hd patients were studied. Each patient underwent a block of six Hd sessions, then was switched to six Hf. During the last session of each dialytic treatment, continuous beat to beat measurements of systolic arterial pressure (SAP) and heart rate (HR) were performed. Spectral analysis of heart rate variability (HRV) was made before and during the treatment to evaluate the modification of autonomic nervous system activity.</AbstractText>Baseline values of plasma sodium, body weight, HR and SAP were not different for the two considered methods of dialysis, while the baseline values of normalized LF were significantly higher in Hf as compared to Hd and the opposite was observed for HF powers (P < 0.001). Sodium balance and body weight loss per hour did not differ between Hd and Hf while body temperature was kept constant in all sessions. Throughout the dialytic procedures, with both techniques, SAP was constant, while HR diminished from the first hour till the end of the procedure (P < 0.05). An increase in LF (and decrease in HF) was noticed only in the case of Hd, considering normalized units (P < 0.05). These selective changes were maintained also during the recovery after the procedure.</AbstractText>The spectral analysis of RR interval variability during Hd and Hf suggests a potential autonomic advantage with Hf, to be added to the well-recognized intrinsic greater haemodynamic stability.</AbstractText>
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2,333,180 |
Adenoviral-mediated expression of dihydropyridine-insensitive L-type calcium channels in cardiac ventricular myocytes and fibroblasts.
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Cardiac voltage-gated Ca2+ channels regulate the intracellular Ca2+ concentration and are therefore essential for muscle contraction, second messenger activation, gene expression and electrical signaling. As a first step in accessing the structural versus functional properties of the L-type Ca2+ channel in the heart, we have expressed a dihydropyridine (DHP)-insensitive CaV1.2 channel in rat ventricular myocytes and fibroblasts. Following isolation and culture, cells were infected with adenovirus expressing either LacZ or a mutant CaV1.2 channel (CaV1.2DHPi) containing the double mutation (T1039Y & Q1043M). This mutation renders the channel insensitive to neutral DHP compounds such as nisoldipine. The whole-cell, L-type Ca2+ current (ICa) measured in control myocytes was inhibited in a concentration-dependent manner by nisoldipine with an IC50 of 66 nM and complete block at 250 nM. In contrast, ICa in cells infected with AdCaV1.2DHPi was inhibited by only 35% by 500 nM nisoldipine but completely blocked by 50 microM diltiazem. In order to study CaV1.2DHPi in isolation, myocytes infected with AdCaV1.2DHPi were incubated with nisoldipine. Under this condition the cells expressed a large ICa (12 pA/pF) and displayed Ca2+ transients during field stimulation. Furthermore, addition of 2 microM forskolin and 100 microM 3-isobutyl-1-methylxanthine (IBMX), to stimulate protein kinase A, strongly increased IBa in the AdCaV1.2DHPi-infected cells. A Cd2+-sensitive IBa was also recorded in cardiac fibroblasts infected with AdCaV1.2DHPi. Thus, expression of CaV1.2DHPi will provide an important tool in studies of cardiac myocyte and fibroblast function.
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2,333,181 |
Time-dependent patterning of the mesoderm and endoderm by Nodal signals in zebrafish.
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The vertebrate body plan is generated during gastrulation with the formation of the three germ layers. Members of the Nodal-related subclass of the TGF-beta superfamily induce and pattern the mesoderm and endoderm in all vertebrates. In zebrafish, two nodal-related genes, called squint and cyclops, are required in a dosage-dependent manner for the formation of all derivatives of the mesoderm and endoderm. These genes are expressed dynamically during the blastula stages and may have different roles at different times. This question has been difficult to address because conditions that alter the timing of nodal-related gene expression also change Nodal levels. We utilized a pharmacological approach to conditionally inactivate the ALK 4, 5 and 7 receptors during the blastula stages without disturbing earlier signaling activity. This permitted us to directly examine when Nodal signals specify cell types independently of dosage effects.</AbstractText>We show that two drugs, SB-431542 and SB-505124, completely block the response to Nodal signals when added to embryos after the mid-blastula transition. By blocking Nodal receptor activity at later stages, we demonstrate that Nodal signaling is required from the mid-to-late blastula period to specify sequentially, the somites, notochord, blood, Kupffer's vesicle, hatching gland, heart, and endoderm. Blocking Nodal signaling at late times prevents specification of cell types derived from the embryo margin, but not those from more animal regions. This suggests a linkage between cell fate and length of exposure to Nodal signals. Confirming this, cells exposed to a uniform Nodal dose adopt progressively more marginal fates with increasing lengths of exposure. Finally, cell fate specification is delayed in squint mutants and accelerated when Nodal levels are elevated.</AbstractText>We conclude that (1) Nodal signals are most active during the mid-to-late blastula stages, when nodal-related gene expression and the movement of responding cells are at their most dynamic; (2) Nodal signals specify cell fates along the animal-vegetal axis in a time-dependent manner; (3) cells respond to the total cumulative dose of Nodal signals to which they are exposed, as a function of distance from the source and duration of exposure.</AbstractText>
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2,333,182 |
Inositol-1,4,5-trisphosphate-mediated spontaneous activity in mouse embryonic stem cell-derived cardiomyocytes.
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Embryonic stem cell-derived cardiomyocytes (ESdCs) have been proposed as a source for cardiac cell-replacement therapy. The aim of this study was to determine the Ca2+-handling mechanisms that determine the frequency and duration of spontaneous Ca2+ transients in single ESdCs. With laser scanning confocal microscopy using the Ca2+-sensitive dye Fluo-4/AM, we determined that spontaneous Ca2+ transients in ESdCs at the onset of beating (day 9) depend on Ca2+ entry across the plasma membrane (50%) whereas Ca2+-induced Ca2+ release is the major contributor to Ca2+ transients in ESdCs after 16 days (72%). Likewise, Ca2+ extrusion in 9-day-old ESdCs depends on Na+-Ca2+ exchange (50.0+/-8%) whereas Ca2+ reuptake by the sarco(endo)plasmic Ca2+ ATPase (72+/-5%) dominates in further differentiated cells. Spontaneous Ca2+ transients were suppressed by the inositol-1,4,5-trisphosphate (IP3) receptor (IP3R) blocker 2-aminoethoxydiphenyl borate (2-APB) and the phospholipase C blocker U73122 but continued in the presence of caffeine. Stimulation of IP3 production by phenylephrine or endothelin-1 had a positive chronotropic effect that could be reversed by U73122 and 2-APB. The presence of Ca2+-free solution and block of L-type Ca2+ channels by nifedipine also resulted in a cessation of spontaneous activity. Overall, IP3R-mediated Ca2+ release in ESdCs is translated into a depolarization of the plasma membrane and a whole-cell Ca2+ transient is subsequently induced by voltage-dependent Ca2+ influx. Although ryanodine receptor-mediated Ca2+ release amplifies the IP3R-induced trigger for the Ca2+ transients and modulates its frequencies, it is not a prerequisite for spontaneous activity. The results of this study offer important insight into the role of IP3R-mediated Ca2+ release for pacemaker activity in differentiating cardiomyocytes.
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2,333,183 |
Laparoscopic cholecystectomy under segmental thoracic spinal anaesthesia: a feasibility study.
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Laparoscopic surgery is normally performed under general anaesthesia, but regional techniques have been found beneficial, usually in the management of patients with major medical problems. Encouraged by such experience, we performed a feasibility study of segmental spinal anaesthesia in healthy patients.</AbstractText>Twenty ASA I or II patients undergoing elective laparoscopic cholecystectomy received a segmental (T10 injection) spinal anaesthetic using 1 ml of bupivacaine 5 mg ml-1 mixed with 0.5 ml of sufentanil 5 microg ml-1. Other drugs were only given (systemically) to manage patient anxiety, pain, nausea, hypotension, or pruritus during or after surgery. The patients were reviewed 3 days postoperatively by telephone.</AbstractText>The spinal anaesthetic was performed easily in all patients, although one complained of paraesthesiae which responded to slight needle withdrawal. The block was effective for surgery in all 20 patients, six experiencing some discomfort which was readily treated with small doses of fentanyl, but none requiring conversion to general anaesthesia. Two patients required midazolam for anxiety and two ephedrine for hypotension. Recovery was uneventful and without sequelae, only three patients (all for surgical reasons) not being discharged home on the day of operation.</AbstractText>This preliminary study has shown that segmental spinal anaesthesia can be used successfully and effectively for laparoscopic surgery in healthy patients. However, the use of an anaesthetic technique involving needle insertion into the vertebral canal above the level of termination of the spinal cord requires great caution and should be restricted in application until much larger numbers of patients have been studied.</AbstractText>
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2,333,184 |
Postoperative analgesia with intravenous fentanyl PCA vs epidural block after thoracoscopic pectus excavatum repair in children.
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The aim of this prospective, randomized trial was to compare analgesia, sedation, and cardiorespiratory function in children after thoracoscopic surgery for pectus excavatum repair, using two types of analgesia--epidural block with bupivacaine plus fentanyl vs patient-controlled analgesia (PCA) with fentanyl.</AbstractText>Twenty-eight patients scheduled for thoracoscopic pectus excavatum surgery were randomly assigned to receive either thoracic epidural block or i.v. PCA for postoperative analgesia. Pain was assessed using a visual-analogue scale (VAS). The Ramsay sedation score, arterial pressure, ventilatory frequency, and heart rate were also measured, and blood gas analysis was performed regularly during the first 48 h after surgery.</AbstractText>A significant decrease in the VAS pain score, Ramsay sedation score, heart rate ventilatory frequency, systolic and diastolic blood pressure, and PaCO2, and a significant increase in PaO2 and oxygen saturation were found over time. Patients in the PCA group had significantly higher PaCO2 values. In addition, a significantly slower decline of systolic blood pressure and heart rate, and faster recovery of PaCO2 were found in PCA patients than in patients with epidural block.</AbstractText>I.V. fentanyl PCA is as effective as thoracic epidural for postoperative analgesia in children after thoracoscopic pectus excavatum repair. Bearing in mind the possible complications of epidural catheterization in children, the use of fentanyl PCA is recommended.</AbstractText>
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2,333,185 |
Ropivacaine versus lidocaine for deep-topical, nerve-block anaesthesia in cataract surgery: a double-blind randomized clinical trial.
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To evaluate the safety and efficacy of ropivacaine versus lidocaine for deep-topical, nerve-block anaesthesia in cataract surgery.</AbstractText>This prospective controlled randomized double-blind study comprised 64 patients undergoing clear corneal phacoemulsification. Patients were equally divided into two group receiving either deep-topical anaesthesia with 1% ropivacaine-soaked sponge (Group R, n = 32) or 2% lidocaine-soaked sponge (Group L, n = 32). The level of intraoperative and postoperative pain was assessed by patients using a verbal analogue scale from 1 to 10. The duration of surgery, the need for supplemental anaesthesia, surgeon satisfaction, and intraoperative and early postoperative complications were recorded. The patients' heart rate, arterial blood pressure and peripheric oxygen saturation (SpO(2)) were obtained just before the anaesthesia and during the surgery.</AbstractText>The demographic data of the patients and duration of surgery were similar in both groups. No significant difference in the mean pain scores of patients were found in the ropivacaine and lidocaine groups. Surgical satisfaction was also statistically insignificant. None of the patients had significant difference in heart rate, blood pressure or SpO(2) during the surgical procedure.</AbstractText>Deep-topical anaesthesia with ropivacaine and lidocaine in cataract surgery is safe and the two anaesthetic agents do not present differences in the degree of analgesia achieved. Deep-topical anaesthesia with ropivacaine or lidocaine was equally effective in providing anaesthesia with sufficient quality for cataract surgery.</AbstractText>
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2,333,186 |
Nonischemic cardiomyopathy associated with autoimmune polyglandular syndrome type II.
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To report a case of nonischemic cardiomyopathy associated with autoimmune polyglandular syndrome type II (APS-II).</AbstractText>We describe our patient's clinical features, evaluation, and outcome. In addition, a literature review of cardiomyopathy associated with polyendocrinopathy syndromes is presented.</AbstractText>The component disorders of APS-II are Addison's disease in combination with either autoimmune thyroid disease or type 1 (insulin-dependent) diabetes. Although numerous other autoimmune conditions have been reported in conjunction with APS-II, cardiomyopathy has not been previously described as part of this syndrome. The current patient was a 32-year-old man who, during a 5-year period, was diagnosed as having type 1 diabetes mellitus, Crohn's disease, and Addison's disease. In 2001, he presented with severe heart failure that progressed rapidly and eventually necessitated cardiac transplantation.</AbstractText>Although autoimmune cardiomyopathy has been associated with other autoimmune disorders, to our knowledge this is the first reported case of cardiomyopathy in association with an autoimmune polyglandular syndrome. Patients with this syndrome should undergo clinical evaluation for heart failure.</AbstractText>
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2,333,187 |
The rise of [Na(+)] (i) during ischemia and reperfusion in the rat heart-underlying mechanisms.
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Intracellular Na(+) concentration ([Na(+)](i)) rises in the heart during ischemia, and on reperfusion, there is a transient rise followed by a return toward control. These changes in [Na(+)](i) contribute to ischemic and reperfusion damage through their effects on Ca(2+) overload. Part of the rise of [Na(+)](i) during ischemia may be caused by increased activity of the cardiac Na(+)/H(+) exchanger (NHE1), activated by the ischemic rise in [H(+)](i). In support of this view, NHE1 inhibitors reduce the [Na(+)](i) rise during ischemia. Another possibility is that the rise of [Na(+)](i) during ischemia is caused by Na(+) influx through channels. We have reexamined these issues by use of two different NHE1 inhibitors, amiloride, and zoniporide, in addition to tetrodotoxin (TTX), which blocks voltage-sensitive Na(+) channels. All three drugs produced cardioprotection after ischemia, but amiloride (100 microM) and TTX (300 nM) prevented the rise in [Na(+)](i) during ischemia, whereas zoniporide (100 nM) did not. Both amiloride and zoniporide prevented the rise of [Na(+)](i) on reperfusion, whereas TTX was without effect. In an attempt to explain these differences, we measured the ability of the three drugs to block Na(+) currents. At the concentrations used, TTX reduced the transient Na(+) current (I (Na)) by 11 +/- 2% while amiloride and zoniporide were without effect. In contrast, TTX largely eliminated the persistent Na(+) current (I (Na,P)) and amiloride was equally effective, whereas zoniporide had a substantially smaller effect reducing I (Na,P) to 41 +/- 8%. These results suggest that part of the effect of NHE1 inhibitors on the [Na(+)](i) during ischemia is by blockade of I (Na,P). The fact that a low concentration of TTX eliminated the rise of [Na(+)](i) during ischemia suggests that I (Na,P) is a major source of Na(+) influx in this model of ischemia.
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2,333,188 |
Correlation between salivary alpha-amylase activity and pain scale in patients with chronic pain.
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The visual analog scale (VAS) is commonly used to assess pain intensity. However, the VAS is of limited value if patients fail to reliably report. Objective assessments are therefore clearly preferable. Previous reports suggest that elevated salivary alpha-amylase may reflect increased physical stress. There is a close association between salivary alpha-amylase and plasma norepinephrine under stressful physical conditions. In this study, we have determined the usefulness of a portable salivary alpha-amylase analyzer as an objective biomarker of stress.</AbstractText>Thirty patients (male/female = 15/15, age: 60.5 +/- 15.3 years) with chronic low back or leg pain (pain (+) group) and 20 pain-free control patients undergoing elective surgery under general anesthesia with epidural analgesia (pain (-) group) were recruited. Patients received epidural block with 5 to 10 mL 1% lidocaine. VAS, blood pressure, and heart rates were assessed before and 30 and 45 minutes after the epidural block. Salivary alpha-amylase was simultaneously measured using a portable analyzer. The relationship between the VAS and salivary alpha-amylase in chronic pain patients was assessed.</AbstractText>After the epidural block both heart rate and systolic blood pressure decreased by approximately 8%. In the pain (+) group, the epidural block markedly decreased the VAS pain scale and salivary alpha-amylase from 56 +/- 22 to 19 +/- 16 mm (P < .01) and from 82 +/- 48 to 45 +/- 28 U/mL (P < .01), respectively, with a significant correlation between the 2 measures (r = 0.561, P < .01). In contrast, salivary alpha-amylase did not change significantly in the pain (-) group.</AbstractText>Because there was a significant correlation between VAS pain scale and salivary alpha-amylase, we suggest that this biomarker may be a good index for the objective assessment of pain intensity. In addition, a simple to use portable analyzer may be useful for such assessment.</AbstractText>
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2,333,189 |
Comparison of 0.25% levobupivacaine, 0.25% bupivacaine, and 0.125% bupivacaine for duration and magnitude of action in peripheral arterial blood flow induced by sympathetic block in dogs.
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The aim of this study is to compare 0.25% levobupivacaine with 0.25% bupivacaine and 0.125% bupivacaine to examine the duration and magnitude of vasodilative effect induced by sympathetic block.</AbstractText>We measured mean arterial pressure (MAP), heart rate (HR), and right and left brachial-artery blood flow (BABF) before and after cervicothoracic sympathetic block in 24 dogs. The experimental protocol was designed as follows: (1) left cervicothoracic sympathetic block with 1.0 mL of 0.25% levobupivacaine (n = 8), (2) left cervicothoracic sympathetic block with 1.0 mL of 0.25% bupivacaine (n = 8), and (3) left cervicothoracic sympathetic block with 1.0 mL of 0.125% bupivacaine (n = 8).</AbstractText>MAP and HR did not change significantly throughout the study in either group. Left cervicothoracic sympathetic block with 0.25% levobupivacaine increased left BABF significantly from 5 minutes through 80 minutes after the block (baseline, 100%; peak at 10 minutes after the block, 185 +/- 35%; P <.01). Left cervicothoracic sympathetic block with 0.25% bupivacaine increased left BABF significantly from 5 minutes through 100 minutes after the block (baseline, 100%; peak at 10 minutes after the block, 251 +/- 47%; P < .01). Left cervicothoracic sympathetic block with 0.125% bupivacaine increased left BABF significantly from 5 minutes through 80 minutes after the block (baseline, 100%; peak at 10 minutes after the block, 155 +/- 20%; P < .01).</AbstractText>0.25% Levobupivacaine may have a lower potency compared with 0.25% bupivacaine in sympathetic block in dogs.</AbstractText>
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2,333,190 |
Vasopressin dysregulation: hyponatremia, fluid retention and congestive heart failure.
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Arginine vasopressin (AVP) plays a central role in the regulation of water and electrolyte balance. Dysregulation of AVP secretion, along with stimulation of AVP V2 receptors, is responsible for hyponatremia (serum sodium concentration <135 mEq/L) in congestive heart failure (CHF). The stimulation of atrial and arterial baroreceptors in response to hypotension and volume depletion results in the nonosmotic release of AVP. The predominance of nonosmotic AVP secretion over osmotic AVP release plays a key role in the development of water imbalance and hyponatremia in CHF and other edematous disorders. The AVP-receptor antagonists are a new class of agents that block the effects of AVP directly at V2 receptors in the renal collecting ducts. AVP-receptor antagonism produces aquaresis, the electrolyte-sparing excretion of water, thereby allowing specific correction of water and sodium imbalance. This review summarizes recent data from clinical trials evaluating the efficacy and safety of these promising agents for the treatment of hyponatremia.
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2,333,191 |
Electrocardiography: the ECG.
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This article examines the role of electrocardiography in patient monitoring during an operative procedure. In addition to providing a wealth of physiological information, including information on the electrical activity of the heart, the ECG assists in monitoring and detecting a variety of changes, such as cardiac arrhythmias, electrolyte changes, and ischemia. Information presented on an ECG should be analyzed systematically with an understanding of the constituent elements of an ECG, the rate, the rhythm, the morphology, the axis, the presence of conduction abnormalities, electrolyte changes, and ischemic changes. To assess accurately the information presented, hemodynamic information and cardiac-risk analysis should be integrated to have a complete picture.
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2,333,192 |
Heart rate and blood pressure variability as markers of sensory blockade with labour epidural analgesia.
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To evaluate the correlation between the progression of somatosensory blockade and changes in autonomic outflow following the onset of labour epidural analgesia.</AbstractText>Twelve labouring parturients consented to participate in the study. Baseline electrocardiogram, blood pressure (BP) and respiratory rate were recorded for ten minutes. The epidural consisted of 0.125% bupivacaine with 50 microg of fentanyl (total volume 20 mL). Measurements were repeated for ten minutes after initiation of the block. The level of sensory block was measured bilaterally with loss of sensation to ice at two-minute intervals. Wavelet transform was used to obtain heart rate (HR) and BP variability every two minutes following the loading dose of epidural medication. High frequency power of HR variability was used to assess changes in parasympathetic activity. The total power of BP variability was used to assess changes in sympathetic activity. A nonparametric repeated measures ANOVA was used for the variability data, and a Spearman rank correlation test was used to evaluate the relationship between the sensory block and HR and BP variability.</AbstractText>The sensory block progressed to T9 at ten minutes post-epidural and was the mirror image of the decrease in total power of BP variability. High frequency power of HR variability increased to a plateau at six minutes post-epidural. A significant correlation was found between the increase in sensory block and the observed decrease in BP variability (r = -1.000, P = 0.0028).</AbstractText>In this study of labouring parturients, BP variability correlated with the progression of both sympathetic and somatosensory block following epidural anesthesia, while HR variability was shown to be a surrogate marker of increased parasympathetic activity.</AbstractText>
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2,333,193 |
A common SCN5A variant alters the responsiveness of human sodium channels to class I antiarrhythmic agents.
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The potential pathophysiological role of common SCN5A polymorphisms in cardiac arrhythmias has been increasingly recognized. However, little is known about the impact of those polymorphisms on the pharmocological response of hNav1.5 to various antiarrhythmic agents.</AbstractText>The known SCN5A polymorphism, S524Y, was studied in comparison with the wild type (WT) in [corrected] the SCN5A-Q1077del variant. The ion channel gating kinetics and pharmacology were evaluated using whole-cell patch-clamp methods in HEK-293 cells. Consistent with a previous report, the basal ion channel gating kinetics of S524Y were indistinguishable from the WT. Quinidine (20 microM) caused similar extent of tonic block reduction of sodium currents at -120 mV in WT and S524Y. Surprisingly, quinidine (20 microM) exerted a more use-dependent block by a 10 Hz pulse train in S524Y than in WT at 22 degrees C (Ki: WT, 51.3 microM; S524Y, 20.3 microM). S524Y significantly delayed recovery from the use-dependent block, compared with the WT (tau= 88.6 +/- 7.9 s vs 41.9 +/- 6.6 s, P < 0.005). Under more physiological conditions using a 2 Hz pulse train at 37 degrees C, S524Y similarly enhanced the use-dependent block by quinidine. In addition, S524Y enhanced the use-dependent block by flecainide (12.5 microM), but not by mexiletine (100 microM).</AbstractText>A common SCN5A polymorphism, S524Y, can enhance a use-dependent block by class Ia and Ic antiarrhythmic agents. Our findings may have clinical implications in pharmacological management of cardiac arrhythmias since this common SCN5A polymorphism might be a contributing factor to the variable antiarrhythmic response.</AbstractText>
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2,333,194 |
Stereoselective block of hERG channel by (S)-methadone and QT interval prolongation in CYP2B6 slow metabolizers.<Pagination><StartPage>719</StartPage><EndPage>728</EndPage><MedlinePgn>719-28</MedlinePgn></Pagination><Abstract><AbstractText>Methadone inhibits the cardiac potassium channel hERG and can cause a prolonged QT interval. Methadone is chiral but its therapeutic activity is mainly due to (R)-methadone. Whole-cell patch-clamp experiments using cells expressing hERG showed that (S)-methadone blocked the hERG current 3.5-fold more potently than (R)-methadone (IC50s (half-maximal inhibitory concentrations) at 37 degrees C: 2 and 7 microM). As CYP2B6 slow metabolizer (SM) status results in a reduced ability to metabolize (S)-methadone, electrocardiograms, CYP2B6 genotypes, and (R)- and (S)-methadone plasma concentrations were obtained for 179 patients receiving (R,S)-methadone. The mean heart-rate-corrected QT (QTc) was higher in CYP2B6 SMs (*6/*6 genotype; 439+/-25 ms; n=11) than in extensive metabolizers (non *6/*6; 421+/-25 ms; n=168; P=0.017). CYP2B6 SM status was associated with an increased risk of prolonged QTc (odds ratio=4.5, 95% confidence interval=1.2-17.7; P=0.03). This study reports the first genetic factor implicated in methadone metabolism that may increase the risk of cardiac arrhythmias and sudden death. This risk could be reduced by the administration of (R)-methadone.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Eap</LastName><ForeName>C B</ForeName><Initials>CB</Initials><AffiliationInfo><Affiliation>Unit of Biochemistry and Clinical Psychopharmacology, Centre for Psychiatric Neurosciences, University Department of Psychiatry-CHUV, Hospital of Cery, Prilly-Lausanne, Switzerland. [email protected]</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Crettol</LastName><ForeName>S</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Rougier</LastName><ForeName>J-S</ForeName><Initials>JS</Initials></Author><Author ValidYN="Y"><LastName>Schläpfer</LastName><ForeName>J</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Sintra Grilo</LastName><ForeName>L</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Déglon</LastName><ForeName>J-J</ForeName><Initials>JJ</Initials></Author><Author ValidYN="Y"><LastName>Besson</LastName><ForeName>J</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Croquette-Krokar</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Carrupt</LastName><ForeName>P-A</ForeName><Initials>PA</Initials></Author><Author ValidYN="Y"><LastName>Abriel</LastName><ForeName>H</ForeName><Initials>H</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016448">Multicenter Study</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2007</Year><Month>02</Month><Day>28</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Clin Pharmacol Ther</MedlineTA><NlmUniqueID>0372741</NlmUniqueID><ISSNLinking>0009-9236</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000701">Analgesics, Opioid</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018076">DNA, Complementary</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000072237">ERG1 Potassium Channel</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051638">Ether-A-Go-Go Potassium Channels</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C000606913">KCNH2 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D026902">Potassium Channel Blockers</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.14.1</RegistryNumber><NameOfSubstance UI="D001189">Aryl Hydrocarbon Hydroxylases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.14.1</RegistryNumber><NameOfSubstance UI="C585599">CYP2B6 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.14.1</RegistryNumber><NameOfSubstance UI="D065702">Cytochrome P-450 CYP2B6</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.5.-</RegistryNumber><NameOfSubstance UI="D010089">Oxidoreductases, N-Demethylating</NameOfSubstance></Chemical><Chemical><RegistryNumber>UC6VBE7V1Z</RegistryNumber><NameOfSubstance UI="D008691">Methadone</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>Clin Pharmacol Ther. 2008 May;83(5):671; author reply 672</RefSource><PMID Version="1">18043689</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000483" MajorTopicYN="N">Alleles</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000701" MajorTopicYN="N">Analgesics, Opioid</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001189" MajorTopicYN="N">Aryl Hydrocarbon Hydroxylases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D065702" MajorTopicYN="N">Cytochrome P-450 CYP2B6</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018076" MajorTopicYN="N">DNA, Complementary</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000072237" MajorTopicYN="N">ERG1 Potassium Channel</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004562" MajorTopicYN="N">Electrocardiography</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051638" MajorTopicYN="N">Ether-A-Go-Go Potassium Channels</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005838" MajorTopicYN="N">Genotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006339" MajorTopicYN="N">Heart Rate</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007700" MajorTopicYN="N">Kinetics</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008133" MajorTopicYN="N">Long QT Syndrome</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="Y">chemically induced</QualifierName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008691" MajorTopicYN="N">Methadone</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010089" MajorTopicYN="N">Oxidoreductases, N-Demethylating</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018408" MajorTopicYN="N">Patch-Clamp Techniques</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D026902" MajorTopicYN="Y">Potassium Channel Blockers</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020133" MajorTopicYN="N">Reverse Transcriptase Polymerase Chain Reaction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013237" MajorTopicYN="N">Stereoisomerism</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2007</Year><Month>3</Month><Day>3</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2007</Year><Month>5</Month><Day>16</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2007</Year><Month>3</Month><Day>3</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">17329992</ArticleId><ArticleId IdType="doi">10.1038/sj.clpt.6100120</ArticleId><ArticleId IdType="pii">6100120</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">17327632</PMID><DateCompleted><Year>2007</Year><Month>06</Month><Day>11</Day></DateCompleted><DateRevised><Year>2008</Year><Month>05</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1512-0112</ISSN><JournalIssue CitedMedium="Print"><Issue>142</Issue><PubDate><Year>2007</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Georgian medical news</Title><ISOAbbreviation>Georgian Med News</ISOAbbreviation></Journal>[Is always chronic total occlusion indication for recanalization in patients with multi-vessel disease].
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Methadone inhibits the cardiac potassium channel hERG and can cause a prolonged QT interval. Methadone is chiral but its therapeutic activity is mainly due to (R)-methadone. Whole-cell patch-clamp experiments using cells expressing hERG showed that (S)-methadone blocked the hERG current 3.5-fold more potently than (R)-methadone (IC50s (half-maximal inhibitory concentrations) at 37 degrees C: 2 and 7 microM). As CYP2B6 slow metabolizer (SM) status results in a reduced ability to metabolize (S)-methadone, electrocardiograms, CYP2B6 genotypes, and (R)- and (S)-methadone plasma concentrations were obtained for 179 patients receiving (R,S)-methadone. The mean heart-rate-corrected QT (QTc) was higher in CYP2B6 SMs (*6/*6 genotype; 439+/-25 ms; n=11) than in extensive metabolizers (non *6/*6; 421+/-25 ms; n=168; P=0.017). CYP2B6 SM status was associated with an increased risk of prolonged QTc (odds ratio=4.5, 95% confidence interval=1.2-17.7; P=0.03). This study reports the first genetic factor implicated in methadone metabolism that may increase the risk of cardiac arrhythmias and sudden death. This risk could be reduced by the administration of (R)-methadone.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Eap</LastName><ForeName>C B</ForeName><Initials>CB</Initials><AffiliationInfo><Affiliation>Unit of Biochemistry and Clinical Psychopharmacology, Centre for Psychiatric Neurosciences, University Department of Psychiatry-CHUV, Hospital of Cery, Prilly-Lausanne, Switzerland. [email protected]</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Crettol</LastName><ForeName>S</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Rougier</LastName><ForeName>J-S</ForeName><Initials>JS</Initials></Author><Author ValidYN="Y"><LastName>Schläpfer</LastName><ForeName>J</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Sintra Grilo</LastName><ForeName>L</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Déglon</LastName><ForeName>J-J</ForeName><Initials>JJ</Initials></Author><Author ValidYN="Y"><LastName>Besson</LastName><ForeName>J</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Croquette-Krokar</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Carrupt</LastName><ForeName>P-A</ForeName><Initials>PA</Initials></Author><Author ValidYN="Y"><LastName>Abriel</LastName><ForeName>H</ForeName><Initials>H</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016448">Multicenter Study</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2007</Year><Month>02</Month><Day>28</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Clin Pharmacol Ther</MedlineTA><NlmUniqueID>0372741</NlmUniqueID><ISSNLinking>0009-9236</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000701">Analgesics, Opioid</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018076">DNA, Complementary</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000072237">ERG1 Potassium Channel</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051638">Ether-A-Go-Go Potassium Channels</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C000606913">KCNH2 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D026902">Potassium Channel Blockers</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.14.1</RegistryNumber><NameOfSubstance UI="D001189">Aryl Hydrocarbon Hydroxylases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.14.1</RegistryNumber><NameOfSubstance UI="C585599">CYP2B6 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.14.1</RegistryNumber><NameOfSubstance UI="D065702">Cytochrome P-450 CYP2B6</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.5.-</RegistryNumber><NameOfSubstance UI="D010089">Oxidoreductases, N-Demethylating</NameOfSubstance></Chemical><Chemical><RegistryNumber>UC6VBE7V1Z</RegistryNumber><NameOfSubstance UI="D008691">Methadone</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>Clin Pharmacol Ther. 2008 May;83(5):671; author reply 672</RefSource><PMID Version="1">18043689</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000483" MajorTopicYN="N">Alleles</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000701" MajorTopicYN="N">Analgesics, Opioid</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001189" MajorTopicYN="N">Aryl Hydrocarbon Hydroxylases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D065702" MajorTopicYN="N">Cytochrome P-450 CYP2B6</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018076" MajorTopicYN="N">DNA, Complementary</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000072237" MajorTopicYN="N">ERG1 Potassium Channel</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004562" MajorTopicYN="N">Electrocardiography</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051638" MajorTopicYN="N">Ether-A-Go-Go Potassium Channels</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005838" MajorTopicYN="N">Genotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006339" MajorTopicYN="N">Heart Rate</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007700" MajorTopicYN="N">Kinetics</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008133" MajorTopicYN="N">Long QT Syndrome</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="Y">chemically induced</QualifierName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008691" MajorTopicYN="N">Methadone</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010089" MajorTopicYN="N">Oxidoreductases, N-Demethylating</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018408" MajorTopicYN="N">Patch-Clamp Techniques</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D026902" MajorTopicYN="Y">Potassium Channel Blockers</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020133" MajorTopicYN="N">Reverse Transcriptase Polymerase Chain Reaction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013237" MajorTopicYN="N">Stereoisomerism</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2007</Year><Month>3</Month><Day>3</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2007</Year><Month>5</Month><Day>16</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2007</Year><Month>3</Month><Day>3</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">17329992</ArticleId><ArticleId IdType="doi">10.1038/sj.clpt.6100120</ArticleId><ArticleId IdType="pii">6100120</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">17327632</PMID><DateCompleted><Year>2007</Year><Month>06</Month><Day>11</Day></DateCompleted><DateRevised><Year>2008</Year><Month>05</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1512-0112</ISSN><JournalIssue CitedMedium="Print"><Issue>142</Issue><PubDate><Year>2007</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Georgian medical news</Title><ISOAbbreviation>Georgian Med News</ISOAbbreviation></Journal><ArticleTitle>[Is always chronic total occlusion indication for recanalization in patients with multi-vessel disease].</ArticleTitle><Pagination><StartPage>39</StartPage><EndPage>41</EndPage><MedlinePgn>39-41</MedlinePgn></Pagination><Abstract>The issue of recanalization chronic total occlusion (CTO) up today stays unsolved. Existence of viable myocardium in the CTO basin is regarded to be one of the proofs in cases of transitory ischemia or in the state of hibernation. But, the question of CTO opening in presence of acinetic segments is still under discussion. The aim of our study is testing assumption that CTO recanalization in the presence of other stenotic arteries, improves global and regional contractility of myocardium. One hundred and twenty patients with MI after one month were enrolled. To diagnose viability of myocardium 72% of patients went through stress-echocardiography with small dozes of dobutimin. After, all patients were divided into two groups: who have to undergo complete revascularization (Group I- 35,5%), and those who have to undergo only CTO revascularization (Group II- 64,5%). There were no significant statistic differences in hemodynamic parameters between groups. In case of multi-vessel disease restoration of antegrade flow in CTO caused to block of CAD attacks and symptoms of congestive heart failure. Therefore, results of the study let us state existence of CTO as indication for angioplasty of infarct-related artery.
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2,333,195 |
Percussion pacing--an almost forgotten procedure for haemodynamically unstable bradycardias? A report of three case studies and review of the literature.
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More than 80 years after its first description by Eduard Schott, percussion (fist) pacing remains a little known procedure even though it represents an instantly available and easy to perform treatment for temporary emergency cardiac pacing in haemodynamically unstable bradycardias, including bradycardic pulseless electrical activity and complete heart block with ventricular asystole. Based on the Consensus on Science and Treatment Recommendations of the International Liaison Committee on Resuscitation, the European Resuscitation Council recently incorporated percussion pacing in its advanced life support guidelines (Nolan and colleagues, Resuscitation 67 (Suppl 1): S39-S86, 2005). Here, we briefly describe three of our own cases and present a review of the literature on percussion pacing with respect to the available evidence on its efficacy, its practical application, and clinical indications.
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2,333,196 |
[Hyperbaric bupivacaine: a randomized double-blind trial of different doses with or without fentanyl for cesarean section under spinal anesthesia].
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To compare the effects of spinal anesthesia with different doses of hyperbaric bupivacaine with or without fentanyl in patients undergoing cesarean section.</AbstractText>Prospective study enrolling 50 ASA 1-2 patients undergoing cesarean section, randomized to 5 treatment groups. Groups A, B, C, and D received 15 microg of fentanyl and group X received no fentanyl. The doses of hyperbaric bupivacaine given in each group were as follows: 10 mg in Group A, 11 mg in group B, 12 mg in group C, 13 mg in group D, and 14 mg in group X.</AbstractText>Patients in groups A and B had greater hemodynamic stability than patients in groups C, D, or X (P < 0.05). The incidence of hypotension was 70% in group C and 80% in groups D and X. The sensory block reached level T4 in groups D and X and the motor block was complete in all cases. Postoperative analgesia lasted longer in group D with a mean (SD) duration of 202 (25) minutes than in group X with a mean duration of 194 (19) minutes. Assessment on a visual analog scale was under 3 in all groups except group A, where 2 patients required administration of propofol.</AbstractText>Acceptable operative conditions with a low incidence of hypotension are provided with an 11 mg dose of hyperbaric bupivacaine.</AbstractText>
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2,333,197 |
Persistence of PAR-2 vasodilation despite endothelial dysfunction in BPH/2 hypertensive mice.
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This study investigated relaxation of vascular smooth muscle by acetylcholine, bradykinin and protease-activated receptor 2 (PAR-2) to characterise endothelial dysfunction in spontaneously hypertensive mice (BPH/2). We hypothesised that PAR-2 induced vasodilation would be preserved in BPH/2 despite the presence of hypertension and impaired vasodilator responses to acetylcholine and bradykinin. Mean arterial blood pressure (MAP), heart rate and locomotor activity were assessed in conscious mice over 24-h periods by radiotelemetry. Relaxation responses of small mesenteric arteries to acetylcholine, bradykinin and the PAR-2 agonist, 2-furoyl-LIGRLO-amide (2fly), were assessed using wire myographs. MAP and heart rate of BPH/2 were 15 and 18%, respectively, higher than in controls (BPN/3). BPH/2 also exhibited increased locomotor activity. Maximal relaxations of arteries by acetylcholine and bradykinin in BPH/2 were reduced by 25-50% relative to BPN/3. In contrast, relaxation responses to 2fly were only slightly (6%), albeit significantly, reduced. Sodium nitroprusside-induced relaxations were not different between strains. Treatment of BPH/2 arteries with inhibitors of calcium-activated K(+) channels was sufficient to block persistent 2fly- and residual ACh- and bradykinin-induced relaxations, whereas NO synthase inhibitor failed to inhibit these relaxations. In BPH/2 mice, vascular smooth muscle relaxation by PAR-2 is well preserved despite the presence of hypertension and impaired vasodilation responses to acetylcholine and bradykinin.
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2,333,198 |
Antiproliferative autoantigen CDA1 transcriptionally up-regulates p21(Waf1/Cip1) by activating p53 and MEK/ERK1/2 MAPK pathways.
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We previously reported that overexpression of cell division autoantigen 1 (CDA1) in HeLa cells arrests cell growth and inhibits DNA synthesis at S-phase. Here we show that CDA1-induced arrest of cell growth is accompanied by increases in protein and mRNA levels of the cyclin-dependent kinase (Cdk) inhibitor protein, p21(Waf1/Cip1) (p21). Both p21 induction and cell growth arrest are reversed when CDA1 expression is inhibited. CDA1 also increases p53 protein, but not its mRNA, in a time- and dose-dependent manner. MDM2, a ubiquitin ligase regulating p53 degradation, is inactivated by CDA1, suggesting that p53 protein accumulation is due to decreased protein degradation. Knockdown of p53, using siRNA targeting two sites of p53 mRNA, abrogates transcriptional induction of p21 by CDA1. Deletion of the p53 responsive element in the distal region of p21 promoter attenuates promoter activity in response to CDA1. DNA damage caused by camptothecin treatment increases mRNA and protein levels of CDA1, accompanied by induction of p53. The DNA damage-induced p53 induction is markedly attenuated by CDA1 knockdown. CDA1 induces phosphorylation of ERK1/2(p44/42), an activity blocked by PD98059 and U0126, inhibitors of the upstream kinase MEK1/2. The MEK inhibitors also block induction of p21 mRNA and abrogate p21 promoter activity stimulated by CDA1. Cell cycle kinases, Cdk1, -2, -4, and -6 are inhibited by CDA1 overexpression. We conclude that CDA1 induces p53- and MEK/ERK1/2 MAPK-dependent expression of p21 by acting through the p53 responsive element in the p21 promoter and that this contributes to its antiproliferative activity.
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2,333,199 |
Observations on the muscle relaxant rocuronium bromide in the horse--a dose-response study.
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To investigate the onset and duration of neuromuscular blockade of rocuronium bromide and its associated haemodynamic effects at three doses in healthy horses.</AbstractText>Prospective, randomized experimental study.</AbstractText>Seven adult horses aged 3-20 (mean 10.3) years and weighing 466 +/- 44 (mean +/- SD) kg.</AbstractText>Horses were anaesthetized three times with at least 2 weeks between. They were pre-medicated with 0.6 mg kg(-1) xylazine and 0.01 mg kg(-1) butorphanol i.v.. Anaesthesia was induced with 2.2 mg kg(-1) ketamine and 0.1 mg kg(-1) diazepam i.v.. Following orotracheal intubation anaesthesia was maintained with isoflurane in 100% oxygen. Intermittent positive pressure ventilation was initiated and the horses were ventilated at a respiratory rate (fr) of 4-8 breaths minute(-1). Neuromuscular function was monitored with an acceleromyograph. The peroneal nerve was stimulated with train-of-four (TOF) mode at 2 Hz every 15 seconds. Each horse received, in randomly assigned order, one of the three doses of rocuronium: 0.2 mg kg(-1) (D02), 0.4 mg kg(-1) (D04) or 0.6 mg kg(-1) (D06) i.v.. Lag time, onset time, time of no response, duration of action and the TOF ratio 0.7 and 0.9 were measured. Recovery time (T1(25-75)) was calculated. Vital parameters were recorded at 5-minute intervals on a standard anaesthetic record form.</AbstractText>Rocuronium produced a dose-dependent duration of action in isoflurane-anaesthetized horses. 100% block was observed in D04 and D06 but not in D02, in which the maximum decrease of the first twitch of TOF attained was 91.5 +/- 16.5%. Time to T1(25) was 13.1 +/- 5.5 minutes, 38.6 +/- 10.1 minutes and 55 +/- 9.8 minutes in D02, D04 and D06 respectively. There was a significantly shorter time for TOFR 0.9 with 0.2 mg kg(-1) compared with 0.4 and 0.6 mg kg(-1) rocuronium. T1(25-75) in D04 and D6 was not statistically significantly different. Heart rate, systolic, diastolic and mean arterial blood pressure increased slightly during the observation period.</AbstractText>Rocuronium is an effective nondepolarizing muscle relaxant in horses under isoflurane anaesthesia. It had a dose-dependent onset and duration of action. Rocuronium did not produce significant changes in the measured cardiovascular parameters.</AbstractText>
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