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采用常现心肌细胞内微电极记录方法，观察钙通道阻滞剂──异搏定在正常台氏液和模拟缺血条件下，对抗溶血磷脂酸胆碱（LPC）的电生理效应。结果显示：3×10-4mol／LLPC能引起类似离体心肌缺血的电生理效应，使静息电位（RP）除极，动作电位振幅（APA）和动作电位0相最大速率（Vmax）降低及动作电位复极至20％、50％、90％的时程（APD20、APD50、APD90）缩短。在模拟缺血条件下，LPC的毒性作用与缺血有协同效应。用10－6mol／L异搏定预处理豚鼠右心室乳头肌标本，在台氏液中有对抗LPC电生理效应（P＜0．05）的作用，但同样浓度的溶液对抗缺血效果不显著（P＞0.05）。因此在缺血条件下抗LPC效应也不理想。
Electrophysiological effects of anti-lysophosphatidylcholine (LPC) on normal cardiomyocytes and in simulated ischemia were observed using the current method of microelectrode recording in cardiomyocytes. The results showed that 3 × 10-4 mol / L LLPC induced electrophysiological effects similar to isolated myocardial ischemia and decreased the resting potential (RP) depolarization, action potential amplitude (APA) and action potential phase 0 maximal velocity (Vmax) And action potential repolarization to 20%, 50%, 90% of the time course (APD20, APD50, APD90) shortened. Under simulated ischemic conditions, the toxic effects of LPC have a synergistic effect with ischemia. Pretreatment of 10-8 mol / L verapamil in guinea pig papillary muscle samples had the effect of antagonizing LPC electrophysiological effect (P <0.05) in Tyrode’s solution, but the same concentration of solution did not significantly inhibit the ischemia (P> 0.05). Therefore, anti-LPC effect is not ideal under ischemic conditions.