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目的:研究关附乙酯(DGFA)对窦房结起搏细胞电生理学的影响.方法:采用细胞内微电极技术记录家兔窦房结动作电位(AP)参数.结果:DGFA不仅能够减慢自主性激发频率(SFF),平均复极化速率(MRR),舒张期除极化速率(RDD),而且以剂量依赖性方式延长窦房结舒张期间隔(DI)和动作电位时程(APD).此外,DGFA显著降低除极化最大速率(MRD),并伴有动作电位幅度(APA)的轻微下降,对最大舒张电位(MDP)无显著作用.DGFA降低自主性激发频率的作用不受阿托品(0.05 mg/L)的影响.结论:DGFA这些作用可能是通过减少钙离于内流及钾离子外流产生的,而非阻断M受体.
Objective: To study the electrophysiological effects of DGFA on pacemaker cells of sinoatrial node.Methods: Intracellular microelectrode technique was used to record the parameters of action potential (AP) of sinoatrial node in rabbits.Results: DGFA not only slowed down (SFF), average repolarization rate (MRR), and diastolic depolarization rate (RDD) in a dose-dependent manner, and prolong the diastolic interval (DI) and action potential duration (APD) In addition, DGFA significantly reduced the maximum rate of depolarization (MRD) accompanied by a slight decrease in APA, with no significant effect on the maximum diastolic potential (MDP). The effect of DGFA on reducing the autonomic excitation frequency was not affected Atropine (0.05 mg / L) .Conclusion: These effects of DGFA may be caused by reducing calcium influx and potassium efflux rather than block M receptor.