急性心肌梗死后一周对心室肌细胞瞬间外向钾电流的影响

研究急性心肌梗死 (AMI)心室肌细胞瞬间外向钾电流 (Ito)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 ,研究AMI后 1周心外膜梗死区心肌细胞Ito的变化。结果 :正常对照组 (n =16 )心肌细胞在 - 30mV激活 ,心肌梗死 (简称心梗 )组细胞在 - 2 0mV激活 ,均呈线性电压依赖性。心梗组梗死区细胞 (n =12 )Ito的电流密度明显下降 ,I V曲线明显下移。心梗组Ito电流密度 (去极化电位 +6 0mV时 )明显低于对照组 (7.4 7± 2 .39vs 17.39± 5 .2 4pA/pF ,P <0 .0 1)。结论 :AMI可引起心室肌细胞Ito电流密度下降 ,导致梗死区细胞动作电位平台期相对延长 ,复极异常 ,造成心肌细胞之间动作电位及不应期离散度增大 ,容易形成折返 ,此可能是导致心肌梗死后出现折返性室性心律失常的原因。

Alteration of Transient Outward Current in Ventricular Myocytes From One-week Acute Infarcted Heart

To study the current density of transient outward current(I to ) in cells from the epicardial infarct zone of the 1 week infarcted rabbit heart,rabbits were infarcted by ligation of the left anterior descending coronary artery.One week later,I to was recorded using patch clamp techniques from infarcted heart(IZs) and compare with the I to from noninfarcted heart(NZs).Results:I to current density(at+60 mv) was significantly reduced in IZs(7.47±2.39 pA/pF, n =12)compared with NZs (17.39±5.24pA/pF, n =16), P <0.01.Conclusion:Our study indicate that there are changes in I to in IZs.These changes may underlie the abnormally long transmembrane action potentials of these arrhymogenic surviving ventricular fibers of the IZs,thus contributing to reentrant ventricular arrhymias in the infarcted heart.