Sodium-hydrogen exchange inhibition during ventricular fibrillation - Beneficial effects on ischemic contracture, action potential duration, reperfusion arrhythmias, myocardial function, and resuscitability
Sodium-hydrogen exchange inhibition during ventricular fibrillation - Beneficial effects on ischemic contracture, action potential duration, reperfusion arrhythmias, myocardial function, and resuscitability
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DOI：
10.1161/01.cir.0000058704.45646.0d
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发表时间：
2003-04-08
期刊：
影响因子：
37.8
通讯作者：
Gazmuri, RJ
中科院分区：
文献类型：
--
作者：
Ayoub, IM;Kolarova, J;Gazmuri, RJ
抑制肌膜钠-氢交换器亚型-1（NHE-1）作为一种有前途的新策略正在出现，用于改善与缺血和再灌注相关的心肌损伤。我们研究了NHE-1抑制是否方法和结果-两组各8只猪接受8分钟未处理的VF，并随机接受3-mg/kg的卡立泊来德或0.9%的卡立泊来德，在常规闭胸复苏的8分钟间隔之前立即给予NaCl。Cariporide阻止了左心室游离壁厚度的进行性增加（NaCl组从1.0+/-0.2至1.5+/-0.3 cm，P
Background-Inhibition of the sarcolemmal sodium-hydrogen exchanger isoform-1 (NHE-1) is emerging as a promising novel strategy for ameliorating myocardial injury associated with ischemia and reperfusion. We investigated whether NHE-1 inhibition (with cariporide) could minimize mechanical and electrical myocardial abnormalities that develop during ventricular fibrillation (VF) and improve outcome using a porcine model of closed-chest resuscitation.Methods and Results-Two groups of 8 pigs each were subjected to 8 minutes of untreated VF and randomized to receive either a 3-mg/kg bolus of cariporide or 0.9% NaCl immediately before an 8-minute interval of conventional closed-chest resuscitation. Cariporide prevented progressive increases in left ventricular free-wall thickness (from 1.0+/-0.2 to 1.5+/-0.3 cm with NaCl, P