内源性腺苷和K_(ATP)通道介导缺氧窦房结起搏细胞的电生理效应(英文)

目的:观察腺苷脱氨酶(ADase),8-苯茶碱(8-PT)和格列苯脲(Gli)在豚鼠缺氧窦房结起搏细胞的电生理效应.方法:以充有100％氮和无糖的K-H液灌流豚鼠窦房结20 min引起其缺氧.用玻璃微电极技术记录起搏细胞的MDP,APA,APD_(90),V_(max),RPF和VDD等动作电位参数.结果:缺氧增加起搏细胞APA,MDP和V_(max),但减小VDD和RPF.Adase 10 U·L~(-1),8-PT 0.1 μmol·L~(-1)和Gli10 μmol·L~(-1)明显缓解缺氧引起的电生理效应. 结论:内源性腺苷和KATp通道在缺氧所致窦房结起搏细胞电生理效应中起重要作用.

Endogenous adenosine and ATP-sensitive potassium channel modulate anoxia-induced electrophysiological changes of pacemaker cells in sinoatrial node of guinea pigs

AIM:To investigate the electrophysiological effects of adenosine deaminase (ADase, an enzyme converting adenosine to inosine and ammonia), 8-phenyltheophylline (8-PT, a non-selective antagonist of adenosine receptors) and glibenclamide (Gli, a potent blocker of ATP-sensitive K channels) on anoxic pacemaker cells of SA node. METHODS: Anoxia of pacemaker cells in SA node of guinea-pig was induced by perfused for 20 min with a modified K-H solution gassed with 100 % N2 deprived of glucose. Parameters of action potentials including maximal diastolic potential (MDP),amplitude of action potential (APA),duration of 90 % repolarization (APD90 ), maximal rate of depolarization (Vmax),rate of pacemaker firing (RPF), and velocity of diastolic (phase 4) depolarization (VDD) were recorded using intracellular mi-croelectrodes. RESULTS: Anoxia increased MDP,APA, and Vmax and decreased VDD, RPF in a time-dependent manner. ADase 10 U.L-1, 8-PT 0. 1 nmol.L-1 and Gli 10 umol .L-1 significantly attenuated the electrophysiological changes of pacemaker cells in sincatri-al node induced by anoxia. CONCLUSION: Endogenous adenosine and ATP-sensitive K channels may play an important role in the generation of anoxic bradycardia in guinea pigs.