兔急性心肌梗死后二月心室肌细胞钠离子通道活性的变化

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。采用结扎兔冠状动脉左前降支的方法建立AMI动物模型 ,应用膜片钳全细胞记录方法 ,观察AMI后 2个月心外膜梗死区心肌细胞钠通道电流 (INa)的变化。结果 :①正常对照组INa电流密度峰值 (去极化电位 - 30mV时 )为 45 .5± 5 .33pA/pF(n =12 ) ,心肌梗死 (简称心梗 )组为 16 .4± 4.43pA/pF(n =13) ,心梗组较对照组明显下降 ,P <0 .0 1。心梗组INa电流 电压关系曲线较对照组明显下移。②心梗组INa失活曲线较对照组明显左移 (即向超级化方向移动 ) ,对照组半数失活电压 (V0 .5)为 - 76 .2± 5 .3mV(n =5 ) ,心梗组V0 .5为 - 82 .4± 5 .6mV(n =12 ) ,P <0 .0 5。③心梗组钠通道灭活后恢复时程较对照组减慢 ,恢复曲线下移。结论 :AMI可导致梗死区心室肌细胞INa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 ,此可能是导致AMI后出现折返性室性心律失常的原因。

Alteration of Na+ Currents in Ventricular Myocytes From Two Months Infarcted Rabbit Heart.

To study the current density and function of Na + channel in cells from the epicardial infarct zone of the two months infarcted rabbit heart,rabbits were infarcted by ligation of the left anterior descending coronary artery, two months later,I Na was recorded using whole cell patch-clamp techniques from infarcted heart(IZs) and compared with the I Na from noninfarcted heart(NZs).Results:Peak I Na current density(at -30 mV) was significantly reduced in IZs(16.4±4.43 pA/pF,n=13)compared with NZs(45.5±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(-82.4±5.6 mV,n=12) compared with NZs (-76.2±5.3 mV,n=5),P<0.05.Recovery of I Na from inactivation was slower in IZs.Conclusion:I Na is 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.