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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.
OBJECTIVE: To observe the electrophysiological effects of adenosine deaminase (ADase), 8-PT and glibenclamide (Gli) on pacemaker cells of hypoxia sinus node in guinea pigs.Methods: 100% nitrogen and sugar-free KH solution perfused sinus node of the guinea pig for 20 min, which caused hypoxia. MDP, APA, APD 90, V max, RPF and VDD of pacemaker cells were recorded by glass microelectrode technique (P <0.05) .Conclusion: Hypoxia can increase the APA, MDP and Vmax of pacemaker cells, but decrease the ratio of VDD and RPF.Adase 10 U · L -1 and 8-PT 0.1 μmol·L -1, And Gli at 10 μmol·L -1 significantly alleviated the electrophysiological effects induced by hypoxia.Conclusion: Endogenous adenosine and KATp channels play an important role in the electrophysiological effects of anoxia on pacemaker cells of sinoatrial node.