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目的:研究杭白菊乙酸乙酯提取物(CME)对大鼠实验性心律失常、心肌易损性与动作电位的影响及其机制。方法:采用乌头碱诱发的整体大鼠心律失常模型研究CME对大鼠实验性心律失常的影响。采用Langendorff离体心脏灌流方法,结扎冠状动脉左前降支30 min后复灌复制局部缺血/复灌模型,测定心肌缺血复灌前后的心室电生理学参数:舒张期兴奋阈(DET)、有效不应期(ERP)、室颤阈(VFT)。采用常规微电极技术记录大鼠右心室乳头肌动作电位,观测静息电位(RP)、动作电位幅度(APA)、有效不应期(ERP)、动作电位的时程(APD90)、动作电位0期最大除极速率(Vmax)。结果:与对照组相比,CME明显降低室性心动过速发生次数,缩短其持续时间,延迟室性早搏、室性心动过速出现时间,心律失常评分显著降低。与对照组相比,CME明显延长离体大鼠心脏的ERP,并对缺血/复灌所致的ERP缩短和VFT降低有明显的减弱作用。与对照组相比,CME明显延长大鼠右室乳头肌动作电位APD50和APD90,降低动作电位Vmax,对动作电位的其他参数影响不显著。结论:CME具有降低大鼠心室易颤性、抗心律失常的作用,其机制可能涉及延长心肌动作电位时程及有效不应期,提高大鼠心脏电生理稳定性。
OBJECTIVE: To study the effects and mechanisms of ethyl acetate extract (CME) of Chrysanthemum morifolium against experimental arrhythmia, myocardial vulnerability and action potential in rats. METHODS: The effect of CME on experimental arrhythmias in rats was studied using aconitine-induced whole rat arrhythmia model. A Langendorff isolated cardiac perfusion method was used to ligate the left anterior descending coronary artery for 30 min and then the model of ischemia/reperfusion was induced by reperfusion. The ventricular electrophysiological parameters before and after myocardial ischemia/reperfusion were determined: diastolic excitation threshold (DET), effective Refractory period (ERP), ventricular fibrillation threshold (VFT). The action potentials of right ventricular papillary muscles were recorded by conventional microelectrode technique. The resting potential (RP), action potential amplitude (APA), effective refractory period (ERP), duration of action potential (APD90) and action potential were observed. Maximum depolarization rate (Vmax). Results: Compared with the control group, CME significantly reduced the number of ventricular tachycardia, shortened its duration, delayed ventricular premature beats, ventricular tachycardia appearing time, arrhythmia score was significantly reduced. Compared with the control group, CME significantly prolonged ERP in isolated rat hearts, and significantly reduced ERP shortening and VFT reduction caused by ischemia/reperfusion. Compared with the control group, CME significantly prolonged the APD50 and APD90 of the right ventricular papillary muscles, decreased the action potential Vmax, and had no significant effect on other parameters of the action potential. Conclusion: CME has the effect of reducing ventricular fibrillation and anti-arrhythmia in rats, and its mechanism may involve prolonging the action potential duration and effective refractory period of myocardium and improving the electrophysiological stability of rat heart.