缺血对心室浦肯野纤维跨膜电位和起搏离子流的影响

采用细胞内微电极和双微电极电压箝制术观察缺血对绵羊心室浦肯野纤维跨膜电位和起搏离子流（Ｉｆ）的影响。结果：模拟缺血液灌流３０ｍｉｎ，浦肯野纤维最大舒张电位（ＭＤＰ）、动作电位幅度（ＡＰＡ）明显减少；动作电位时程ＡＰＤ５０，ＡＰＤ９０明显缩短（ｎ＝１５Ｐ＜０．０１）；起搏离子流（Ｉｆ），幅度降低，激活曲线向超极化方向移位，最大激活时间及半最大激活时间延长（ｎ＝１３Ｐ＜０．００１）。上述结果表明：心肌缺血时，心室浦肯野细胞跨膜电位及正常起搏活动不是增强，而是减弱。提示缺血性室性心律失常不是由于正常心室自律活动异常增强引起

EFFECT OF ISCHEMIA ON THE TRANSMEMBRANE POTENTIAL AND THE PACEMAKER CURRENT IN CARDIAC PURKINJE FIBERS

We have employed two microelectrode voltage clamp technique to detect the effect of ischemia mimic solution on the transmembrane potential and the pacemaker current (I f) in sheep cardiac purkinje fibers. The sequence was as follow: after being perfused with ischemia mimic solution, the maximun diastolic potential (MDP)and the action potential amplitude(APA) were decreased, the action potential duration (APD) was shortened significantly ( n =15, P <0. 01);the amplitude of I f was decreased, the activation curve of I f was shifted to hyperpolarization direction, the activation time and half activation time to a steady state value of I f current were prolonged ( n =l3, P <0.01). The above results indicated that under the ischemia condition, the transmembrane potential and the pacemaker function of cardiac purkinje cell are inhibited, and acute ischemia ventricular arrhythmia may not be caused by abnormal strengthening of normal ventricular pacemaker activity.