急性心肌梗死对心室肌细胞钾电流的影响

Alteration of transient outward K^+ current and inward rectifier K^+ current in ventricular myocytes from acute infarcted heart

目的 :研究急性心肌梗死 (AMI)心室肌细胞瞬时外向钾电流 (Ito)和内向整流性钾电流 (IK1 )的变化。方法 :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 ,记录比较 AMI后 1周心外膜梗死区心肌细胞 Ito和 IK1 的变化。结果 :心梗组 Ito明显下降 ,I- V曲线明显下移。指令电位为 +60 m V时 ,Ito在心梗组为 1.0 8± 0 .2 4n A(n=12 ) ,与对照组 (2 .0 9± 0 .3 9n A ,n=16)相比 ,显著下降 ,P<0 .0 1;心梗组 IK1 与对照组比较 ,明显下降 ,特别在超极化时。指令电位为 - 12 0 m V时 ,心梗组 IK1 为 3 .0 1± 0 .49n A (n=11) ,对照组为 4.12±0 .5 1n A(n=10 ,P<0 .0 5 )。结论 :AMI可引起心室肌细胞 Ito和 IK1 的下降 ,从而导致动作电位平台期延长、复极异常 ,这可能是导致

AIM:To study the change in transient outward K + current(I to ) and inward rectifier K + current(I K1 ) 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,I to and I K1 were recorded by using patch clamp techniques from infarcted heart (IZs) and compared with the noninfarcted heart (NZs). RESULTS:I to (at +60 mV) was significantly reduced in IZs(1.08±0.24 nA, n =12) compared with NZs(2.09±0.39 nA, n =16), P <0.01;I K1 (-120 mV) was also significantly reduced in IZs (3.01±0.49 nA, n =11) compared with NZs(4.12±0.51 nA, n =10), P <0.05. CONCLUSION:There were changes in both I to and I K1 in IZs, which changes might underlie the abnormal long transmembrane action potentials and repolarization of these arrhymogenic surviving ventricular fibers of the IZs. Thus contributing to reentrant arrhymias in the infarcted heart.