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在氨基甲酸乙酯麻醉家兔心肌缺血／再灌注模型上，观察了ＡＴＰ敏感性钾（ＫＡＴＰ）通道开放剂Ｃｒｏｍａｋｌｉｍ（Ｃｒｏ）和预缺血对血流动力学和心肌梗塞范围的影响，旨在阐明ＫＡＴＰ通道是否参与预缺血对缺血／再灌注心肌的保护机制。所得结果如下：①单纯缺血３０分钟－再灌注１８０分钟过程中，血流动力学各参数和心肌耗氧量均进行性降低，心肌梗塞范围为３２．３％。②静脉注射Ｃｒｏ后再进行缺血／再灌注时，心肌梗塞范围２３．３％，较单纯缺血／再灌注组明显减小（Ｐ＜０．０５），表明ＫＡＴＰ通道激活对缺血／再灌注心肌有保护作用。③预缺血后，心肌梗塞范围为２１．６％，与单纯缺血／再灌注组相比，有明显差异（Ｐ＜０．０１）；而ＫＡＴＰ通道特异性阻断剂格列苯脲则可阻断预缺血对缺血／再灌注心肌的保护效应，提示ＫＡＴＰ通道在预缺血心肌保护过程中起重要作用。以上结果表明，ＫＡＴＰ通道参与预缺血对心肌的保护机制。
Effects of ATP-sensitive potassium channel (KATP) channel opener Cromaklim (Cro) and ischemic preconditioning on hemodynamics and infarct size were observed in a urethane anesthetized rabbit model of myocardial ischemia / reperfusion. To elucidate whether KATP channels are involved in the protection of ischemic / reperfused myocardium by ischemic preconditioning. The results are as follows: ① Ischemia for 30 minutes - During 180 minutes of reperfusion, parameters of hemodynamics and myocardial oxygen consumption were decreased progressively. The range of myocardial infarction was 32.3%. (2) The incidence of myocardial infarction ranged from 23.3% after ischemia / reperfusion, which was significantly lower than that of ischemia / reperfusion group (P <0.05), indicating that activation of KATP channel was associated with ischemia / reperfusion Perfusion myocardial protection. ③ After ischemic preconditioning, myocardial infarction ranged from 21.6%, which was significantly different from that of ischemia / reperfusion group (P <0.01); while KATP channel blocker glibenclamide Can block the protective effect of precontraction on myocardial ischemia / reperfusion, suggesting that KATP channel plays an important role in the process of ischemic preconditioning. The above results indicate that KATP channels are involved in the protective mechanism of precontraction on myocardium.