【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)30min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κ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(cTnI)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<0.05)。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。更多还原

【Abstract】 Objective To investigate the role of κ receptor in the cardioprotective 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 (cTnI) 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.更多还原