杭白菊乙酸乙酯提取物对大鼠实验性心律失常的影响及其机制

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.

Antiarrhythmic effect of ethyl acetate extract from Chrysanthemum Morifolium Ramat on rats

Objective: To investigate the effect of ethyl acetate extract from Chrysanthemum Morifolium Ramat (CME) on experimental arrhythmia induced by ischemia/reperfusion or aconitine in rats and to explore its underlying mechanisms. Methods: Arrhythmia model in intact rat was induced by aconitine (30 μg/kg body weight,i.v.).In isolated Langendorff perfused rat hearts,regional ischemia and reperfusion was induced by ligation and release of left anterior descending artery.The ventricular fibrillation threshold (VFT),effective refractory period (ERP),and diastolic excitation threshold (DET) in the isolated heart were measured.The action potentials of papillary muscle in rat right ventricle were recorded by conventional glass microelectrode technique. Results: Compared with control group CME significantly decreased the number and duration of ventricular tachycardia (VT);delayed the occurrence of ventricular premature beats (VPB) and VT induced by aconitine.Arrhythmia score of the CME group was lower than that in aconitine-treated group.CME markedly prolonged the ERP and increased the VFT in the isolated perfused rat hearts during ischemia and reperfusion.CME prolonged action potential duration at 50% and 90% repolarization of the right ventricular papillary muscles and decreased the maximal rate of rise of the action potential upstroke,but did not affect the resting potential,amplitude of action potential. Conclusion: CME can reduce myocardial vulnerability and exerts its antiarrhythmic effects induced by aconitine or ischemia/reperfusion,which may be related to its prolongation of action potential duration and effective refractory period that enhance the electrophysiological stability of myocardiaium.