伊布利特对低钾诱发豚鼠心律失常的电生理效应

目的:探讨伊布利特对低钾性左心室流出道慢反应自律细胞电生理的影响。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+伊布利特(0.01mg/ml)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),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),并出现心律不齐;在低钾灌流液组中加入伊布利特可明显延缓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,而伊布利特能拮抗低钾诱发的心律失常,降低诱发所导致的自发放电频率的升高,提示伊布利特对治疗低钾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。

Electrophysiological Effects of Ibutilide on arrhythmia in guinea pigs with Hypokalemia

Objective： To study the electrophysiology Effects of Ibutilide on hypokalemia of guinea pigs. and to investigate the antiarrhythmie effect of Ibutilide. Methods： We recorded the action potentials by conventional intraeellular microelectrode technique and observe the amplitude of action potential （APA） and maximal rate of depolarization （Vmax） and 50%, 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 Ibutilide group. Results： Compared with normal controls, action potential of APD50,APD90 of left ventricular outflow tract pacemaker cells in hypokalemia group were decreased （P〈0. 05） , APA ,Vmax,and RPF significantly increased （P〈0. 01）, and there existed arrhythmia, Ibutilide （0. 0 1mg/ml ）could significantly prolong APD50, APD90 （P（0.05） ; significantly decreased APA , Vmax, and RPF （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 hypokalemia , and Ibutilide can counteract arrhythmia induced by hypokalemia, the therapeutic mechanism may be related to the regulation of the slow response trieular outflow tract abnormalities.