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【目的】研究血红素氧合酶‐1（HO‐1）和线粒体ATP敏感性钾（Mitochondrial KATP ，mitoKATP ）通道与吗啡预处理的延迟性心肌保护作用的关系。【方法】雄性Wistar大鼠随机分为5组。IR组（A组），腹腔注射生理盐水5 mL ，24 h后行心肌缺血再灌注（IR）；Mor组（B组），腹腔注射吗啡3 mg／kg（用生理盐水稀释至5 mL），24 h后行心肌IR；HO‐1阻滞剂（ZnPP‐IX）＋ Mor组（C组），腹腔注射ZnPP‐IX 20μg／kg ，30 min后腹腔注射吗啡3 mg／kg ，24 h后行心肌IR；mitoKATP通道阻滞剂（5‐HD）＋Mor组（D组），腹腔注射5‐HD 5 mg／kg ，20 min后腹腔注射吗啡3 mg／kg ，24 h后行心肌IR；Mor＋5‐HD组（E组），腹腔注射吗啡3 mg／kg ，24 h后行IR ，但在缺血前10 min腹腔注射5‐HD 5 mg／kg。各组于缺血前、缺血25 min、再灌注30、60、120 min记录大鼠心率（HR ）、平均动脉压（MAP）。心肌缺血再灌注结束即刻采用 EB ／TTC双重染色，称重法测定心肌梗死面积，比较各组心肌梗死面积发生情况。【结果】和A组相比，B组心肌梗死面积明显减小，且差异有显著性（ P＜0．05）；C组、D组和E组心肌梗死面积无明显差异（ P ＞0．05）。【结论】HO‐1和mitoKATP通道参与了吗啡预处理的延迟性心肌保护作用；mitoKATP通道既是启动因子又是效应器。“,”[Objective] To explore whether heme oxygenase‐1 (HO‐1) and mitochondrial ATP sensitive potas‐sium (mitoKATP ) channel are involved in morphine‐induced delayed cardioprotection .[Methods] Wistar rats were randomly divided into 5 groups .And 25 min regional ischemia plus 2 h reperfusion (IR) at 24 h post‐treatment of 0 .9% sodium chloride 5 mL in group IR;morphine 3mg/kg in group Mor ;HO‐1inhibitor ZnPP‐IX 20μg/kg plus morphine 3 mg/kg in group ZnPP+ Mor;mitoKATP channel antagonist 5‐hydroxydecanoic acid (5‐HD) 5 mg/kg plus morphine 3 mg/kg in group 5‐HD+Mor .In group Mor+5‐HD ,IR 24 h after morphine 3mg/kg and 10 min after 5‐HD 5 mg/kg .Heart rate (HR) and mean arterial blood pressure (MAP) were recorded at pre‐ischemia , 30 ,60 ,120 min post‐reperfusion .Infarct size (percentage area at risk) was assessed at the end of reperfusion .[Results] No statistical differences in HR or MAP existed among five groups .Infarct size was 60 .0% ± 10 .5% in group IR .Pretreatment with morphine reduced infarct size to 27 .4% ± 8 .2% after 24 h in group Mor .The reduc‐tion of infarct size by morphine was abolished by 5‐HD given either before morphine application or before ischemia . And cardioprotection was abolished by ZnPP‐IX given before morphine in group ZnPP+Mor .[Conclusion]Both HO‐1 and mitoKATP are probably involved in delayed cardioprotection evoked by morphine .And mitoKATP channel may serve as both a trigger and a effector in cardioprotection .