中文摘要：

目的：研究血红素氧化酶1的诱导剂高铁血红素在对抗大鼠心肌缺血-复灌损伤中的作用及其相应机制。方法：利用离体大鼠心脏Langendorff灌流模型，观察心功能、心肌梗死面积等指标的变化。结杲：腹腔注射高铁血红素后24h，可明显改善缺血-复灌心脏（30min缺血／2h复灌）的收缩功能，减少复灌期乳酸脱氢酶（LDH）和肌酸磷酸（CK）的释放，缩小心肌梗死面积。在腹腔注射高铁血红素前给予线粒体Katr通道阻断剂5-HD或肌膜KAtr通道阻断剂HMR-1098均可取消高铁血红素引发的心肌保护作用。在高铁血红素预处理后24h，缺血／复灌前10min给予Kca通道阻断荆paxilline，与高铁血红素组相比，心肌梗死面积扩大，心脏收缩功能下降。结论：高铁血红素预处理可对抗心肌缺血-复灌性损伤，其作用可能与激活KATP通道和KCa通道有关。

英文摘要：

Objective： To investigate the effects of heme oxygenase 1 inducer hemin on protection of ischemia-reperfusion injury in rats and its mechanisms. Methods： The Langendorff model of isolated rat heart was used; the left anterior descending coronary artery was occluded for 30 min and subsequently reperfused for 2 h. Then the ventricular function and infarct size were measured. Results： Heroin preconditioning prevented the increase in LVEDP,decrease in LVDP and ＋dp/dtmax in the isolated ischemia-reperfusion rat hearts. The leakage of LDH and CK in the coronary effluent was significantly declined in hemin-treated rat hearts. And the infarct size was also reduced. Administration of a blocker of mitochondrial ATP-sensitive potassium channel （mitOKATP） 5-HD （5 mg/kg） before hemin preconditioning increased the LVEDP,and reduced the LVDP and ±dp/dtmax. The leakage of LDH and CK in the coronary effluent and the infarct size were also increased compared with only hemin-treated rat hearts. Pretreatment of the rats with a blocker of sarcolemmal ATP-sensitive potassium channel （sarcKART） HMR-1098 （6 mg/kg） before heroin preconditioning also abolished the protective effect. Infusion of paxilline （1μmol/ L）,a blocker of calcium activated potassium channel （Kca） for 10 rain before ischemia/reperfusion led to larger infarct size and poorer myocardial performance as compared with the heroin group. The leakage of LDH and CK in the coronary effluent was also increased. Conclusion： Both mitoKATP and sarcKATP channels activation are required for the delayed cardioprotection induced by hemin. The opening of KCa channels-dependent mechanism may be involved in the protection.