急性心肌梗死1周和8周后心室肌细胞瞬间外向钾电流的变化

ALTERATION OF TRANSIENT OUTWARD K^+ CURRENT IN VENTRICULAR MYOCYTES FROM 1-8 WEEK INFARCTED RABBIT HEART

目的探讨急性心肌梗死后心外膜梗死区心肌细胞瞬间外向钾电流的变化 ,以及心律失常的发生机制。方法采用结扎兔冠状动脉左前降支的方法建立急性心肌梗死动物模型 ,应用膜片钳全细胞记录方法 ,记录急性心肌梗死后 1和 8周心外膜梗死区心肌细胞瞬间外向钾电流的变化。结果瞬间外向钾电流密度 (+6 0mV)的对比显示 :梗死后 1周组和梗死后 8周组均显著低于对照组 (P均 <0 .0 1) ,但梗死后 8周组较梗死后 1周组有明显增高 (P <0 .0 5 )。结论急性心肌梗死可引起心室肌细胞瞬间外向钾电流密度下降 ,从而导致动作电位平台期延长 ,复极异常 ,可能是导致急性心肌梗死后出现折返性室性心律失常的原因 ;在急性心肌梗死后 8周这种电生理异常有恢复趋势。

ObjectiveTo study the current density of transient outward K + current(I to ) in cells from the epicardial border zone of 1 and 8 week infarcted rabbit hearts.MethodsRabbits were infarcted by ligation of the left anterior descending coronary artery,post myocardial infarction 1 week(PMI 1w) as well as 8 week(PMI 8w)later, I to was recorded using whole cell patch clamp techniques from infarcted heart and compared with the I to from non infarcted heart(control). ResultsI to current density (at +60 mV) was significantly reduced in PMI 1w and PMI 8w was compared with control(P< 0.01 ). Nevertheless, there was a significant increase in PMI 8w compared with PMI 1w(P< 0.05 ). ConclusionThere are changes in I to after coronary artery occlusion.These changes may underlie the abnormally long transmembrane action potentials of these arrhymogenic surviving ventricular fibers of the infarcted hearts,thus contributing to reentrant arrhymias in the infarcted hearts. By 8 weeks after occlusion,the depressed I to had returned to near normal, suggesting the presence of reverse remodeling.