Pacing-induced heart failure causes a reduction of delayed rectifier potassium currents along with decreases in calcium and transient outward currents in rabbit ventricle
Pacing-induced heart failure causes a reduction of delayed rectifier potassium currents along with decreases in calcium and transient outward currents in rabbit ventricle
复制标题
DOI：
10.1016/s0008-6363(00)00180-2
复制
发表时间：
2000-11-01
影响因子：
10.8
通讯作者：
Kodama, I
中科院分区：
文献类型：
--
作者：
Tsuji, Y;Opthof, T;Kodama, I
目的：心衰患者和动物模型与心室肌细胞动作电位延长有关。一些膜电流的变化已经被证明是这种延长的基础。然而，关于延迟整流钾电流（I-K）的两个组成部分（I-Kr和I-Ks）在快速起搏引起的心力衰竭中缺乏信息。方法与结果：10只家兔左心室起搏350 ~ 380次/分，连续3 ~ 4周，分别记录左心室顶端肌细胞的动作电位、全细胞电流、I-K、I-tol、I-Kl、ICa-L。与333和1000 ms的周期长度相比，衰竭心脏的肌细胞在90%复极时的动作电位持续时间（APD(90)）延长。衰竭心脏心肌细胞中对e -4031敏感和耐药的I-K成分（I-Kr, I-Ks）均显著低于对照心脏；去极化至+50 mV后，I-Kr和I-Ks的尾电流密度分别为0.62+/-0-05和0.96+/-0.12 pA/pF
Objective: Heart failure in patients and in animal models is associated with action potential prolongation of the ventricular myocytes. Changes in several membrane currents have been already demonstrated to underlie this prolongation. However, information on the two components (I-Kr and I-Ks) of the delayed rectifier potassium current (I-K) in rapid pacing induced heart failure is lacking. Methods and results: Action potentials and whole-cell currents, I-K, I-tol, I-Kl, and ICa-L were recorded in apical myocytes of left ventricle from 10 rabbits subjected to left ventricular pacing at 350-380 beats/min for 3-4 weeks and 10 controls with shan operation. Action potential duration at 90% repolarization (APD(90)) was prolonged in myocytes from failing hearts compared to controls at both cycle lengths of 333 and 1000 ms. Both E-4031-sensitive and -resistant components of I-K (I-Kr, I-Ks) in myocytes from failing hearts were significantly less than those of control hearts; tail current densities of I-Kr and I-Ks following depolarization to +50 mV were 0.62+/-0-05 vs. 0.96+/-0.12 pA/pF (P