摘要
为探讨在急性心肌梗死 (AMI)早期瞬间外向钾通道的变化及其在室性心律失常发生中的作用 ,以开胸冠状动脉 (简称冠脉 )结扎法制备兔急性心肌缺血模型 ,1h后处死动物分离心室肌细胞 ,采用全细胞膜片钳记录技术观察缺血区心外膜心室肌细胞瞬间外向钾通道电流 (Ito)的变化 ,以正常心肌Ito为对照。结果 :急性冠脉结扎 1h兔缺血区心室肌细胞Ito受到抑制 ,电流密度$C电压关系曲线下移 ,测试电压 + 60mV时的Ito电流密度对比显示 :对照组为 1 7.39± 5 .2 4pA/pF (n =1 2 ) ,冠脉结扎 1h组为 7.75± 3.1 1pA/pF (n =1 0 ) ,与对照组相比下降了 5 7% ,P <0 .0 0 1 ;其失活曲线左移 ,半数最大失活电压 (V1 /2 )对照组为 - 35 .2± 5 .3mV(n =1 2 ) ,冠脉结扎 1h组为 - 5 5 .1± 5 .6mV(n =1 0 ) ,与对照组比较失活速度加快 ,P <0 .0 1 ;冠脉结扎后 1h组Ito恢复明显减慢 ,恢复时程延长 ,P <0 .0 5。结论 :冠脉结扎后 1h缺血区心室肌细胞瞬间外向钾通道受抑制 ,影响动作电位复极 ,容易诱发 2相折返 ,可能为AMI后室性心律失常发生的机制之一。
To determine the changes of transient outward potassium currents(I to ) of rabbit ischemic myocytes after acute myocardial infarction(AMI). Rabbit models were made by ligation of branches of left coronary artery. After 1 hour, single ventricular myocytes were isolated enzymatically from ischemic zone, the normal cells from similar region in normal rabbit hearts. I to was recorded by using patch clamp techniques in the whole cell configuration. Results: I to at +60 mV from ischemic cells in the coronary occluded group was significantly reduced (7.75±3.11 pA/pF, n =10) compared to cells from control group (17.39±5.24 pA/pF, n =12), P <0.001, the I to density decreased 57%. The steady state inactivation curve was shifted to the hyperpolarizing direction in ischemic cells, the half maximal voltage dependence of inactivation(V 1/2 ) was -55.1±5.6 mV in ischemic cells and -35.2±5.3 mV in the control cells. Conclusion: Inhibitation of I to is found in the ischemic cells and might be important in the development of ventricular arrhythmias after AMI.
出处
《中国心脏起搏与心电生理杂志》
2003年第4期287-290,共4页
Chinese Journal of Cardiac Pacing and Electrophysiology
关键词
急性心肌梗死
心室肌细胞
瞬间外向钾电流
膜片钳
电生理学
Electrophysiology Rabbit Myocardial infarction, acute Cardiomyocyte Patch clamp Transient outward potassium current
