中文摘要：

目的：研究苦参碱对低钙诱发豚鼠左心室流出道心律失常的电生理影响及苦参碱抗心律失常作用。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、低钙灌流液、和低钙＋苦参碱（50μmol/l）灌流液对豚鼠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）,4相自动去极速度（Vmax）,舒张期除极速率（VDD）,50%复极化时间（APD50）,90%复极化时间（APD90）,自发放电频率（RPF）的影响。结果：与正常对照组相比,低钙灌流液组左心室流出道慢反应自律细胞20min后MDP下降,APA升高,Vmax明显加快（P〈0.05）;VDD明显增快,APD50、APD90均明显缩短（P〈0.01）,RPF显著变快（P〈0.01）并出现阵发性心律不齐;此时在低钙灌流液组中加入苦参碱（50μmol/l）可明显延缓APD50、APD90（P〈0.01）;并使APA、Vmax缩短（P〈0.05）、RPF逐渐变慢（P〈0.01）,稳定20min后,自发放电频率（RPF）基本恢复正常的节律。结论：低钙可明显影响豚鼠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,而苦参碱能拮抗低钙诱发的心律失常,降低诱发所导致的自发放电频率的升高,提示苦参碱对治疗低钙性左心室流出道慢反应自律细胞异常电生理所诱发的心律失常有显著疗效。

英文摘要：

To study the electrophysiology Effects of Matrine on hypocalcemia of guinea pigs and to investigate the antiarrhythmic effect of Matrine. Methods： We recorded the action potentials by conventional intracellular microelectrode technique and observe the amplitude of action potential（APA） and maximal rate of depolarization （ Vm,~） and 50% ,90% of duration of action potential（ APDs0 and APD90 ） and the rate of potential frequency （RPF） in guinea pigs left ventricular outflow tract pacemaker cells of normal control group,hypocalcemia group and hypocalcemia adding Matrine group（ 50p.mol/ 1）. Results： Compared with normal controls, action potential of APDs0,APDgo of left ventricular outflow tract pacemaker cells in hypocalcemia group were decreased （ P 〈 0.01 ） , APA , Vmaxincreased （ P 〈 0. 05 ） , and RPF significantly increased （P 〈 0. 01 ） , and there existed arrhythmia,The addition of Matrine （50μmol/L） can significantly prolong APDs0 ,APDgo （P 〈 0.05 ） ; APA, Vmax decreased （ P 〈 0. 05 ） and RPF significantly decreased （ P 〈 0.01 ） , 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 can be influenced by hypocalcemia, and Matrine can counteract arrhythmia induced by hypocalcemia,suggesting that the therapeutic mechanism of Matrine for the treatment of arrhythmia induced by hypocalcemia is related to the regulation of the slow response of left ventricular outflow tract abnormalities.