Abstract: Objective：To investigate the role of mitochondrial ATP-sensitive potassium channel (mito-KATP) in delayed preconditioning with sevoflurane reducing oxidative injury induced by myocardial ischemia-reperfusion in rats. Methods：Sixty healthy male SD rats were randomly divided into 5 groups (n = 12): the sham operating group (Sham), the ischemia-reperfusion group (IR), the sevoflurane preconditioning group ( SPC), the sevoflurane preconditioning + 5-hydroxydecanoate group (SPC +5-HD)and the 5-hydroxydecanoate group (5-HD). Serum cTnI were detected at the end of reperfusion and myocardial infarct size(IS) were measured by triphenyltetrazolium chloride（TTC）staining. The Ca2 + levels and malondialdehyde (MDA) content in the myocardium were determined. The activity of superoxide dismutase (SOD) and glutathione S-transferase (GST) was measured. Western blot assay was used to assess the expression of glutathione S-transferase Mu (GSTM) expression in the left ventricle. Results： After ischemia-reperfusion,IR group indicated a significant increase of infarct size ,serum cTnI release, myocardial MDA and Ca2+ content, but a decreased activity of SOD, GST and myocardial GSTM expression (P＜0.01).SPC attenuated the infarct ratio and cTnI release, down-regulated myocardial MDA and Ca2+levels， but up-regulated SOD and GST activity and myocardial GSTM abundance(P＜0.01). As compared with SPC group, SPC+5-HD group increased infarct size, serum cTnI levels, myocardial MDA and Ca2+ content, but decreased SOD , GST activity and myocardial GSTM (P<0.01). Conclusion：Delayed preconditioning with sevoflurane can reduce oxidative injury induced by myocardial ischemia-reperfusion, in which mito-KATP is an important regulator.

Key words: anesthetics, inhalation, myocardial reperfusion injury, ischemic preconditioning, myocardial, glutathione transferase, mitochondrial proton-translocating atpases, 心肌梗死