摘要
本实验观察了外源性自由基对大鼠左室乳头肌细胞电生理活动的影响。实验发现,(1)活性氧OH^-、O_2^-、H_2O_2均能抑制心肌细胞动作电位振幅(APA)。其中,OH^+组由给药前的110.5±11.8降至98.0±10.4mV,H_2O_2组由112.3±13.2降至99.0±13.6mV,O_2^-组由117.2±14.5降至103.8±13.2mV(P<0.05),(2)OH^+与H_2O_2能降低动作电位的0相上升最大速率(V_(max)),给药前后相比均有显著性差异(P<0.05)。0_2^-与OH^-、H_2O_2不一样,它增加V_(max)(P<0.05);(3)OH^+组还降低静息电位(RP),而H_2O_2组与O_2^-组尽管亦减小其RP,但给药前后相比无显著性差别。三种活性氧成分均不影响动作电位时程。自由基清除剂过氧化氢酶可对抗自由基降低APA、V_(max)等的抑制效应,起到保护作用。实验结果提示心肌缺血再灌注性心律失常原因之一可能与自由基改变心肌细胞电生理活动有关。
Standard microelectrode technique was used to study the effect of external free radical generating system (EFR) on action potential of papillary muscle cells of 48 Wistar male rats. EFR were produced from activated oxygen systems: including hydrogen peroxide (H_2O_2), hydroxyl (OH^-) and superoxider (O_2^-). The experiment was divided into six groups: a). control, b). OH^-, c). O_2^-, d). H_2O_2, e). OH^-+catalase(CAT, 150U/ml, f). H_2O_2+CAT and the data were analysed on-line by a computer (Apple Ⅱ Doctor-851). The results showed: (1). a highly significant reduction in action potential amplitude in group OH^- (from 110.5±11.8mV to 98.0±10.4mV), H_2O_2 (from 112.3±13.2mV to 99.0±13.6mV) and O_2^+ (from 117.2±14.5mV to 103.8±13.2mV). (2). a significant decrease in maxium rate of depolariztion (Vmax) respectively (P<0.05) in group OH^- and H_2O_2 but an increase in group O_2^- (p<0.05). (3) a highly significant reduction in resting potential in group OH^- (P<0.05). These changes could be prevented by adding free radical scavenger-CAT to the bath. It is concluded that free radicals produced during myocardial ischemia and reperfusion might play an important role in developing arrhythmias.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1991年第1期58-62,共5页
Chinese Journal of Pathophysiology
关键词
心律失常
自由基
动作电位
Free radicals
Action potentials
Arrhythmia
Catalase