大鼠缺血后中层心室肌细胞钠通道改变的实验研究

Experimental Study on Changes of Na^+ Channel in Midmyocardial Myocytes After Simulated Ischemia in Rabbits

【目的】探讨中层心室肌细胞钠通道在缺血性心律失常发生中的作用及其机制。【方法】以酶解法分离中层心室肌细胞,并采用全细胞膜片钳记录技术,观察灌流正常细胞外液后以及灌流缺血外液后10min、20min、30min的快钠电流(INa)的大小及动力学变化。【结果】缺血后INaIV曲线上移,缺血前及缺血后10min、20min、30min的峰电流密度在中层细胞(n=18cells)依次为(31.46±13.72)、(17.45±2.71)、(11.21±4.90)、(8.26±6.39)pA/pF(P<0.05)。缺血后失活曲线左移,失活半电压在缺血前及缺血后10min、20min、30min在中层细胞(n=18cells)依次为(-103.00±8.67)、(-106.30±2.31)、(-114.30±1.89)、(-135.00±5.10)mV(P<0.05)。缺血后INa的灭活后恢复减慢,但无显著性差异(P>0.05)。【结论】缺血时中层心室肌细胞钠通道活性的变化可影响心肌兴奋性和传导性,为心律失常发生的机制之一。

[Objective]To study the role of Na channel of midmyocardium in ischemic arrhythmias. [Methods]Single myocytes were enzymatically isolated from midmyocardium of the free wall of left ventricle, then Na^＋ current INa of midmyocardial myocytes （superfused with normal and then ischemia solution） were recorded using the whole-cell patch-clamp techniques. Compared the current densities and kinetics of Na＋ current INa before and after 10 minutes, 20 minutes, 30 minutes simulated ischemia. [Resuhs]After ischemia, the I-V curves of INa in midmyocardium were significantly shifted upward, and the inactivation curves of INa were significantly shifted to the hyperpolarizing direction（ P〈0.05）. The peak current densities before and after 10 minutes, 20 minutes, 30 minutes simulated ischemia were （31.46±13.72）,（17.45±2.71） ,（11. 21±4.90）, （8.26± 6.39） pA/pF, respectively. And the half-maximal inactivation voltages were （ - 103.00 ± 8.67 ）, （ - 106.30±2. 31） ,（-114.30±1.89） ,（-135.00±5.10） mV. The recoveries from INa inactivation in midmyocardium were slightly decreased, but without significance, [Conclusion]The alteration of Na channel of midmyocardium in simulated ischemia can affect the excitability and conductivity of myocardium. This is one of the mechanisms of arrhythmias.