目的探讨苦参碱对低钾致兔左心室流出道细胞电生理异常保护作用及其机制.方法应用常规玻璃微电极细胞内记录技术,观察正常灌流液、低钾灌流液、低钾+苦参碱(50μmol/L)灌流液对兔左心室流出道慢反应自律细胞最大舒张电位(MDP),动作电位0相幅值(APA),50%复极化时间(APD50),90%复极化时间(APD90),4相自动去极速度(Vmax),自发放电频率(RPF)的影响.结果与正常对照组相比,低钾灌流液组左心室流出道慢反应自律细胞20min后APD50、APD90均明显缩短(P〈0.05);APA、Vmax、RPF显著变快(P〈0.01);在低钾灌流液组中加入苦参碱可明显延缓APD50、APD90(P〈0.05);并使APA缩短、Vmax、RPF逐渐变慢(P〈0.01),稳定20min后,RPF基本恢复正常的节律.结论低钾可明显影响兔左心室流出道慢反应自律细胞电活动,使其自律性发生改变,而苦参碱能拮抗这种作用,降低低钾诱发所导致的RPF的升高,提示苦参碱对低钾性左心室流出道慢反应自律细胞具有明显的电生理保护作用.
Objective To study the electrophysiology effects of Matrine on hypokalemia of guinea pigs left ventricular outflow tract cells.Methods The action potentials were recorded by conventional intracellular microelectrode technique,while the amplitude of action potential(APA),maximal rate of depolarization(Vmax),50% and 90% of duration of action potential(APD50 and APD90) and the rate of potential frequency(RPF) in guinea pigs left ventricular outflow tract pacemaker cells of normal control group,hypokalemia group and hypokalemia adding Matrine group were observed.Results Compared with the results of normal controls,action potentials of APD50、APD90 of left ventricular outflow tract pacemaker cells in hypokalemia group were decreased(P0.05),APA、Vmax、and RPF significantly increased(P0.01),and there existed arrhythmia.The addition of Matrine(50 μmol/L)could significantly prolong APD50、APD90(P0.05);APA、Vmax、and RPF significantly decreased(P0.01).Twenty minutes after reperfusion,spontaneous dischange frequency recovered to the normal control rhythm.Conclusion the result indicates that the automaticity of left ventricular outflow tract pacemaker cells can be influenced by hypokalemia and Matrine can counteract abnormal electrophysiology induced by hypokalemia.