缺血后处理对大鼠心室肌细胞内向整流钾电流和动作电位的影响

目的探讨缺血后处理(IPC)对大鼠心室肌细胞内向整流钾电流(IK1)和动作电位的影响及机制。方法实验分IPC组、缺血/再灌注(I/R)组、单纯灌流(SP)组,利用大鼠心脏建立离体灌注模型,采用胶原酶酶解法分离得到大鼠单心室肌细胞,采用膜片钳全细胞技术分别记录三组心室肌细胞电流和动作电位的变化。结果在-120mV和-30mV刺激电压水平,IK1电流密度:IPC组低于I/R组,I/R组高于SP组(P均<0.05),IPC组同SP组无差异(P>0.05)。与SP组和IPC组比较,I/R组静息电位明显升高(P<0.05);而动作电位幅度、20%动作电位时程、50%动作电位时程、90%动作电位时程均明显下降(P<0.05)。而IPC组各值与SP组无差异(P>0.05)。结论IPC可以降低大鼠缺血/再灌注心肌细胞IK1,延长缺血/再灌注心肌细胞APD。

Effects of ischemic postconditioning on intward rectifier potassium current and action potential of ventricular myocytes of rats

Objective To investigate the effects and the mechanism of ischemic postconditioning(IPC) on intward rectifier potssium current IK1 and action potential of ventricular myocytes of rats.Methods Ventricular myocytes were singly isolated from rat heart using modified Langendoff perfusion and soaked with collagenase.IK1 and action potential of single rat ventricular myocytes were recorded by whole-cell path-clamp technique.Result The density of IK1 in both IPC group and simple perfusion(SP)group were lower than that in ischemia /reperfusion(I/R)group(P< 0.05).The resting membrane potential of I/R group was higher than that in both IPC group and SP group(P<0.05).The action potential amplitude,APD20,APD50,APD90 of I/R group were shorter than that in both IPC group and SPgroup(P<0.05).There was no significant difference between IPC group and SP group in both the density of IK1 and action potential.Conclusion IPC can reduce the density of IK1 and prolong the APD of ischemia /reperfusion ventricular myocytes of rats.