阿片受体、蛋白激酶C和ATP敏感性钾通道介导吗啡预处理的延迟性心肌保护

Opioid receptor,protein kinase C and KATP channel mediate morphine-induced late phase of preconditioning

目的研究阿片受体、蛋白激酶C和ATP敏感钾通道是否介导了吗啡预处理的延迟性心肌保护作用。方法 64只新西兰大白兔均分为单独应用阿片受体(OR)阻断药纳洛酮(A组)、蛋白激酶C(PKC)阻断药白屈菜红碱(B组)、ATP敏感钾通道阻断药格列苯脲(C组)或分别联合吗啡预处理组(D、E、F组)后进行心肌缺血-再灌注,并与吗啡预处理组(G组)、生理盐水对照组(H组)比较,以心肌梗死范围为指标判断心肌损伤程度。结果 G组心肌梗死面积明显小于H组(P<0.01)。A、B、C组以及D、E、F组心肌梗死面积与H组差异无统计学意义。结论阿片受体、蛋白激酶C和ATP敏感钾通道介导了吗啡预处理的延迟性兔心肌保护作用。

Objective To test if the late phase of preconditioning induced by morphine is mediated by opioid receptor, protein kinase C and KAVP channel. Methods Sixty-four New Zeland rabbits were divided 8 groups with 8 rabbits each. All rabbits were subjected 30 min myocardial ischemia and 2 hours reperfusion（I- R）. The rabbits in group H or group G were given normal saline or morphine 24 h before I-R. Naloxone and chelerythrine were given alone in groups of A and B or before morphine pretreatment in group D and group E. Glibenclamide was given at 24 h after morphine pretreatment but before ishemia in group F, or given alone before isehemia in group C. Myocardial infarct size was determined to evaluate the severity of I-R injury. Results Myocardial infarct size was decreased by morphine pretreatment. Naloxone, chelerythrine and glibenclamide given alone had no effect on myocardial infarct size, but they abolished morphine-induced myocardioprotection. Conclusion Opioid receptor, protein kinase C and KATP channel mediate late phase myocardial protection produced by morphine preconditioning in rabbits.