中文摘要：

目的探讨κ受体在芬太尼后处理和肢体远隔缺血后处理（RIP）心肌保护作用机制中的作用。方法将72只成年雄性SD大鼠随机均分为四组：模型组、芬太尼后处理组、肢体RIP组、芬太尼后处理和肢体RIP联合应用组。全部大鼠在体结扎冠状动脉左前降支（LAD）30rain和再灌注180min。在结扎LAD前5min，将每组再均分为A、B两个亚组，分别静脉输注生理盐水和-受体拮抗剂nor-binaltorphimine（nor-BNI）。再灌注180min时，测定血浆肌酸激酶MB同工酶（CK-MB）活性和血清心肌肌钙蛋白I（cTnl）浓度，采用伊文氏蓝和氯化三苯基四氮唑染色法测定心肌梗死面积（IS）。结果芬太尼后处理和肢体RIP均可显著降低心肌缺血-再灌注后的IS以及血清CK—MB和cTnI（P〈0．05），联合应用组心肌保护效果显著增强（P〈O．05）。结论κ受体参与芬太尼后处理的心肌保护作用，但未参与肢体RIP的降低进行梗死面积的保护作用。κ受体对于联合应用芬太尼后处理和肢体RIP降低心肌梗死面积方面的协同作用十分重要。

英文摘要：

Objective To investigate the role of κreceptor in the cardioproteetive effects by fentanyl postconditioning and limb remote ischemic postconditioning （RIP）. Methods Seventy-two anesthetized male SD rats were randomly allocated equally into four groups （n= 18 in each group） ： control group, fentanyl postconditioning group, RIP group, and combined fentanyl postconditioning and RIP group. Rat was opened chest and the left anterior descending coronary artery （LAD） was encircled with a suture to make a snare. All the rats received a 30-min ischemia by LAD ligation and a 180-min reperfusion by LAD open in vivo. Five mintes before LAD ligation, all the rats in each group were divided into the two subgroups the saline （subgroup A） or nor-binaltorphimine （nor-BNI） （subgroup B）. Infarct size was determined by 2, 3, 5-triphenyltetrazolium chloride staining. The serum levels of creatine kinase isoenzyme MB （CK-MB） and cardiac troponin I （eTnI） in plasma were measured at the end of reperfusion. Results Both fentanyl postconditioning and RIP significantly decreased the infarct size, CK-MB and cTnI levels induced by ischemia-reperfusion（P%0.05）, and these effects were enhanced by fentanyl postconditioning plus RIP （P〈 0.05）. Conclusion The κ-opioid receptor is involved in the cardioprotection of fentanyl postconditioning, but not in RIP, and it plays an important role in the synergistic effect in combiaed fentanyl postconditioning and RIP.