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本文用双微电极电压箝制术观察“缺血”及毒性代谢产物溶血磷脂酸胆碱（LPC）对绵羊心室浦肯野纤维起搏离子流If的影响。用模拟缺血溶液灌流15，30和60min后，在一60mV～120mV之间的各不同指令电位水平If离子流幅值均降低（n=5，P＜0．05），激活达稳态时间及半激活时间延长（n=5，P＜0．05），稳态激活曲线向超极化方向移位。在正常台氏液中加入2×10-5mol/LIPC，灌流后，各个膜电位水平的浦氏纤维起搏离子流If的幅值显著降低（n=10，P＜0.05），稳态激活曲线向超极化方向移位，但If激活达稳态时间及半激活时间均无明显改变。在模拟缺血溶液灌流30min基础上，再加2×10－5mol／LLPC灌流，15min后测得If幅值进一步减小（n=10，P＜0．05），加剧了“缺血”对If离子流的抑制作用。上述结果表明：缺血代谢产物溶血磷脂酸胆碱对心室的正常自律活动具有抑制作用，在模拟缺血条件下，它能使已受抑制的自律活动抑制进一步加深。因此它的存在不会异常增强心室自律性活动而发生快速性室性心律失常。
In this paper, double-electrode voltage clamp technique was used to observe the effect of “ischemia” and lysophosphatidylcholine (LPC), a metabolite of lysophosphatidylcholine (LPC), on myocardial pacing current If in sheep ventricular Purkinje fibers. After perfusion with simulated ischemic solution for 15, 30, and 60 min, the amplitude of If currents decreased at different command potentials (60 mV ~ 120 mV) (n = 5, P <0.05) And half activation time (n = 5, P <0.05). The steady-state activation curve shifted to hyperpolarization. In normal Tyrode’s solution, 2 × 10-5 mol / L IPC was added. After perfusion, the amplitude of the Pulsed Fibers Pacing Flow If at each membrane potential decreased significantly (n = 10, P <0.05) To the direction of hyperpolarization shift, but If activation reaches the steady-state time and half activation time no significant change. On the basis of simulating ischemia perfusion for 30min and perfusion of 2 × 10-5mol / LLPC, if amplitude was further decreased after 15min (n = 10, P <0.05), aggravating the “ischemia” If ion flow inhibition. The above results indicate that the ischemic metabolite lysophosphatidylcholine has an inhibitory effect on ventricular normal autonomic activity, which further inhibits the inhibition of self-regulatory activity under simulated ischemic conditions. Therefore its presence does not abnormally enhance ventricular self-regulatory activity and rapid ventricular arrhythmia.