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:【目的】探讨KATP通道在心肌缺血预适应 (IP)中的作用。【方法】用膜片钳单通道记录技术的细胞贴附式研究急性短暂缺氧复氧对新鲜分离的豚鼠心肌细胞细胞膜KATP通道影响。【结果】短暂缺氧 10min可明显引起细胞膜KATP通道的开放 ,缺氧诱导的KATP通道的开放以簇状开放为主。复氧 2min及用 2mmol/LATP可抑制通道开放 ,其电导值为 89 7pS。缺氧使通道开放概率 (Po)明显增加 ,并可诱发通道出现二级开放。【结论】短暂缺氧可以激活心肌细胞膜KATP通道的开放 ,说明心肌细胞膜KATP通道参与了IP的保护作用。
: 【Objective】 To investigate the role of KATP channel in myocardial ischemic preconditioning (IP). 【Method】 Patch-clamp single-channel recording technique was used to study the effect of acute transient hypoxia-reoxygenation on KATP channels of freshly isolated guinea pig cardiomyocytes. 【Results】 The transient hypoxia 10 min obviously induced the opening of KATP channel, and the opening of hypoxia-induced KATP channel dominated cluster opening. Reoxygenation 2min and 2mmol / LATP can inhibit the channel opening, the conductance value of 89 7pS. Hypoxia significantly increased the probability of open channel (Po) and induced secondary open channel. 【Conclusion】 The transient hypoxia can activate the opening of KATP channel in myocardial cell membrane, indicating that the myocardial cell membrane KATP channel is involved in the protective effect of IP.