预处理对缺血再灌注时心肌电生理的影响

目的探讨缺血预适应（IPC）对缺血/再灌注心律失常的影响及其机制。方法12只犬随机分为对照组（n=6）和IPC组（n=6）,采用特制电极记录技术,观察和测量三层心肌单相动作电位（MAP）及有效不应期（ERP）,分析室性心律失常发生率、MAP时程（MAPD）、MAPD跨室壁离散（TDR）及ERP跨室壁离散（TDE）。结果对照组6只中有4只发生室速/室颤,而IPC组6只中仅1只发生室速/室颤。对照组缺血时MAPD同步缩短,而ERP延长且三层心肌延长的幅度不一致,再灌注时逐步恢复。IPC组缺血时MAPD缩短与ERP延长均不明显,与对照组相比,具有显著差异（P<0.05）。各组三层心肌之间的MAPD是一致的。对照组缺血/再灌注时ERP明显不一致,TDE增大,而IPC组TDE小,两者相比较具有显著差异（P<0.05或P<0.01）。结论IPC减少缺血/再灌时MAPD、ERP的变化及TDE,这可能是其抗心律失常的部分机制。

Effect of preconditioning on myocardium electrophysiology during ischemia/reperfusion

AIM To explore the effect and mechanism of which ischemic preconditioning(IPC) protect against arrhythmias induced by ischemia/reperfusion(IR).METHODS Twelve-canines were divided into two groups randomly: control(IR) group and IPC(a single 5 min occlusion and 10 min reperfusion followed by IR) group.With the monophasic action potential(MAP) technique,MAP duration and effective refractory period(ERP) of the three layers myocardium were measured by specially designed plunge-needle electrodes.The incidence of ventricular arrhythmias,transmural dispersion of repolarization(TDR) and transmural dispersion of ERP(TDE) were analyzed.RESULTS In the control group,four of six occurred with ventricular tachycardia/ventricular fibrillation,but one of six occurred with ventricular tachycardia/ventricular fibrillation in IPC group.In the control group,MAP duration shortened similarly,but ERP lengthened in different altitude among the three layers myocardium during ischemia,which was restored during reperfusion.In IPC group,Both MAP duration and ERP did not change obviously,and compared with control group,the difference was statistically significant(P<0.05).Among of the three layers myocardium,MAP duration was uniform in two groups.In control group,compared with IPC group ERP changed obviously and TDE increased during IR(P<0.05 or P<0.01).(CONCLUSION) IPC can reduce both MAP duration shortening and ERP lengthening concomitant with TDE during IR,which may be a part of the electrophysiological mechanism by which IPC protects against the arrhythmias induced by IR.