线粒体在δ阿片药物性心肌冬眠保护复苏后心功能作用中的研究  

The Role of Mitochondira during δ Opioid Induced Pharmacological Myocaridal Hibernation Protecting Postresuscitation Dysfunction

作　　者：方向韶[1] 李恒[1] 符岳[1] 黄子通[1] 

机构地区：[1]中山大学孙选仙纪念医院急诊科,510120

出　　处：《岭南急诊医学杂志》2009年第6期427-429,432,共4页Lingnan Journal of Emergency Medicine

基　　金：广东省自然科学基金资助项目(8151008901000100);广东省医学科学研究基金资助项目(B2007048)

摘　　要：目的:在线粒体水平研究心跳骤停与心肺复苏期间,激动δ阿片受体诱导药物性心肌冬眠保护复苏后心功能的机制。方法:交流电致颤法诱发大鼠心室颤动,8min的室颤后开始包括胸外按压和机械通气的心肺复苏,6min后电击除颤。动物随机分为3组:(1)心肺复苏组;(2)δ阿片受体激动剂组;(3)δ阿片受体拮抗剂+δ阿片受体激动剂组。δ阿片受体拮抗剂在室颤前15min预先给药,δ阿片受体激动剂或者生理盐水在室颤5min时给药。动态监测血流动力学,在复苏成功后6h处死动物电镜观察心肌线粒体损伤情况。结果:δ阿片受体激动剂组复苏后心功能明显改善,δ阿片受体拈抗剂预处理完全取消其保护作用;和心肺复苏组和8阿片受体拮抗剂组相比较,δ阿片受体激动剂组动物心肌的线粒体超微结构的完整性明显保存完好。结论:在心跳骤停与心肺复苏期间激动δ阿片受体诱导药物性心肌冬眠通过保护心肌线粒体超微结构的完整性,从而减轻复苏后心功能损伤。Objective: To investigate the potential mechanism by which δ opioid induced pharmacological myocaridal hibernation protects the heart during cardiac arrest and cardiopulmonary resuscitation (CPR) in the level of mitochondria. Methods: Sprague-Dawley rats were electrically induced ventricular fibrillation (VF). CPR including mechanical ventilation and chest compression was initiated after 8 min of untreated VF.After an additional 6 min of CPR administration, defibrillation was attempted. The animals were randomly divided into three groups:1)CPR group, 2) δ opioid agonist group and 3)δ opioid agonist pretreated with the opioid receptor-blocking agent naloxone group. opioid receptor antagonist was injected 15 min before induction of VF. Either the δ opioid receptor agonist or saline placebo was injected into the right atrium after 5 min of untreated VF. Hemodynamic parameters were observed and ultrastructure examination of r at heart mitochondria was performed. Results: The postresuscitation dysfunction was significantly improved in the δ opioid agonist group. The benefit myocardial protective effect induced by δ opioid receptor was abolished by pretreated with the opioid receptor-blocking agent. The ultrastructure integrity of mitochondria was more intact in the δ opioid agonist group compared with the CPR and naloxone pretreatment group. Conclusion: The protective effect of postresuscitation function confered by δ opioid induced pharmacological myocaridal hibernation was mediated via protecting the integrity of mitochondiral ultrastructure during the cardiac arrest and CPR.

关 键 词：线粒体超微结构 阿片受体激动剂 药物性 心肌冬眠 保护 心肺复苏 功能作用 阿片受体拮抗剂 心肌线粒体 心功能 心跳骤停 受体诱导 心室颤动 完整性 复苏期 动物 min 血流动力学 预先给药 胸外按压 

分 类 号：R459.7[医药卫生—急诊医学]