背景 心肌缺血再灌注损伤(Myocardial ischemia-reperfusion injury, MIRI)能够引起严重的后果。虽然，缺血或药物预处理、缺血或药物后处理等处理方法均能达到心肌保护的作用，但是其心肌保护机制有待深入研究。目的 总结三磷酸腺苷-敏感性钾（Adenosine Triphosphate sensitive potassium , KATP ）通道及其心肌保护作用机制的研究进展。内容 各种心肌保护方法能够直接开放KATP通道或通过激活G蛋白耦联受体间接开放KATP通道。与此同时，开放的KATP通道能够于再灌注早期刺激产生活性氧物质（Reactive Oxygen Species , ROS ）及关闭线粒体通透性转换孔(Mitochondrial Permeability Transition Pore , mPTP )等方式减轻MIRI。趋向 各种心肌保护的方法需要广泛应用于实践，其包括KATP通道通道在内的各种机制需要更深入地研究。
Background: Myocardial ischemia-reperfusion injury (MIRI) could cause serious consequences. Although it was found that ischemic/pharmacological preconditioning and ischemic/pharmacological postconditioning could exert protectional effects against MIRI , myocardial protection mechanisms needed to be further researched. Objective: To conclude ATP sensitive potassium channels and their research progress of myocardial protection mechanism. Content: Studies have shown that when those protectional measures were carried out, ATP sensitive potassium channels could be stimulated to be open directly or indirectly by activating the G protein-coupled receptor. Furthermore, it was found that upregulated reactive oxygen species (ROS) and closed mitochondrial permeability transition pores during the early period of reperfusion were involved in the protectional mechanisms of opening ATP sensitive potassium channels. Trend: If all kinds of methods of myocardial protection want to be widely used in practice, a variety of mechanisms of their methods, including ATP sensitive potassium channels, need to be further studyed.
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