论文部分内容阅读
目的:观察银杏酮酯(GBE50)对正常及模拟缺血豚鼠乳头肌动作电位的影响,探讨GBE50的抗心肌缺血作用。方法:运用标准微电极细胞内记录技术观察GBE50对正常及模拟缺血豚鼠乳头肌动作电位参数(RP,APA,OS,APD20,APD50,APD90)的影响。结果:20,50,100 mg.L-1GBE50缩短心室乳头肌APD50和APD90(P<0.05),且呈剂量依赖性,而对其他参数没有影响;模拟缺血液灌流使RP,APA,OS分别减小,APD20,APD50,APD90分别缩短,而在缺血液中加入100 mg.L-1GBE50,缺血20 min仅APA缩短,其他参数无变化。结论:在生理状态下,GBE50可轻微缩短APD。在缺血状态下动作电位各项参数均减小,而GBE50通过维持缺血期间膜电位的稳定性,对抗缺血对跨膜电位的抑制效应,从而达到抗心肌缺血作用。
Objective: To observe the effect of GBE50 on the action potentials of papillary muscles in normal and simulated guinea pigs, and to explore the anti-ischemic effects of GBE50. Methods: Standard microelectrode intracellular recording technique was used to observe the effect of GBE50 on the action potential parameters (RPA, APA, OS, APD20, APD50, APD90) of normal and simulated guinea pig papillary muscles. Results: 20,50,100 mg.L-1GBE50 shortened APD50 and APD90 (P <0.05) in a dose-dependent manner and had no effect on other parameters. Simulated ischemic perfusion decreased RP, APA and OS, APD20, APD50 and APD90 were shortened respectively. However, only 100 mg.L-1GBE50 was added to ischemic solution, APA was shortened only 20 minutes after ischemia, and no change was observed in other parameters. Conclusion: Under physiological conditions, GBE50 can slightly shorten APD. Under ischemic conditions, the parameters of action potentials decreased, while GBE50 could prevent the ischemic transmembrane potential by maintaining the stability of membrane potential during ischemia, thus achieving anti-ischemic effect.