Ionic mechanism of action potential prolongation in ventricular myocytes from dogs with pacing-induced heart failure
Ionic mechanism of action potential prolongation in ventricular myocytes from dogs with pacing-induced heart failure
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DOI：
10.1161/01.res.78.2.262
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发表时间：
1996-02-01
影响因子：
20.1
通讯作者：
Tomaselli, GF
中科院分区：
文献类型：
--
作者：
Kaab, S;Nuss, HB;Tomaselli, GF
在人类心力衰竭中已经描述了膜电流异常。为了确定在大型心力衰竭动物模型中是否观察到类似的电流变化，我们研究了患有起搏诱导的心肌病的狗。从13只快速心室起搏3 ~ 4周引起心力衰竭的犬和16只非起搏对照犬的中层心肌中分离的心肌细胞在细胞表面积或静息膜电位方面没有差异。然而，从衰竭心室分离的心肌细胞动作电位时程（APD）显著延长（90%复极时APD为1097+/-73毫秒[衰竭心脏，n=30]对842+/-56毫秒[对照心脏，n=25]; P
Membrane current abnormalities have been described in human heart failure. To determine whether similar current changes are observed in a large animal model of heart failure, we studied dogs with pacing-induced cardiomyopathy. Myocytes isolated from the midmyocardium of 13 dogs with heart failure induced by 3 to 4 weeks of rapid ventricular pacing and from 16 nonpaced control dogs did not differ in cell surface area or resting membrane potential. Nevertheless, action potential duration (APD) was significantly prolonged in myocytes isolated from failing ventricles (APD at 90% repolarization, 1097+/-73 milliseconds [failing hearts, n=30] versus 842+/-56 milliseconds [control hearts, n=25]; P