急性心肌梗死后1周兔心室肌细胞钠离子通道活性的变化

目的:研究急性心肌梗死(AMI)后心室肌细胞钠离子通道活性的变化。方法:采用结扎兔冠状动脉左前降支方法建立AMI动物模型, 应用膜片钳全细胞记录方法, 观察AMI后1周心外膜梗死区心肌细胞钠通道电流(I_Na)的变化。结果:正常对照组I_Na电流密度峰值(-30mV)为(45.5±5.33)PA/PF(n=12), 心梗组为(22.48±4.62)PA/PF(n=14), 明显低于对照组, P＜0.01, I_Na电流-电压关系曲线在心梗组明显下移;心梗组I_Na失活曲线较对照组明显左移, 对照组V_0.5为(-76.2±5.3)mV(n=5), 心梗组为(-89.1±5.6)mV(n=6), P＜0.05;心梗组钠通道灭活后恢复时程明显慢于对照组, 恢复曲线下移。结论:AMI可导致梗死区心室肌细胞I_Na下降、钠通道动力学发生变化, 引起心肌传导速度下降和不应性延长, 可能是导致AMI后出现折返性室性心律失常的原因。

Alteration of Na+ currents in ventricular myocytes from 1-week infarcted rabbit heart

AIM:To study the current density and function of Na⁺ channel in cells from the epicardial border zone of the 1-week infarcted rabbit heart.METHODS:Rabbits were infarcted by ligation of the left anterior descending coronary artery.1 week later, INa was recorded using whole cel patch-clamp techniques in ventricular my ocytes from infarcted heart(IZs)and compared with the INa from noninfarcted heart(NZs).RESULTS:Peak I_Na current density(at -30 mV) was significantly reduced in IZs(22.48±4.62 PA/PF, n=14) compared with NZs(45.50±5.33 PA/PF, n=12), P＜0.01;V_0.5 of the availability curve(I/Imax curve)was shifted significantly in the hyperpolarizing direction in IZs(-89.1±5.6 mV, n=6) compared with NZs (-76.2±5.3 mV, n=5), P＜0.05.Recovery of I_Na from inactivation was significantly slower in IZs.CONCLUSIONS:I_Nais reduced, and its kinetics are altered in IZs.These changes may underlie the altered excitability and postrepolarization refractoriness of ventricular fibers of the IZs, thus contributing to reentrant arrhymias in the infarcted heart.