异氟烷预处理对离体大鼠浅低温缺血再灌注心肌线粒体耐受性的影响  

Isoflurane-preconditioning induced mitochondrial tolerance in the rat heats under moderate hypothermic ischemia

作　　者：钱丽萍[1] 朱珊珊[1] 曾因明[1] 

机构地区：[1]徐州医学院江苏省麻醉学重点实验室,221002

出　　处：《国外医学（麻醉学与复苏分册）》2005年第3期129-133,共5页Foreign Medical Sciences(Anesthesilolgy and Resuscitation)

基　　金：江苏省自然科学基金资助项目(BK2002139)

摘　　要：目的探讨异氟烷预处理能否诱导浅低温缺血再灌注心肌线粒体耐受。方法采用SD大鼠离体心脏Lange-ndroff灌注模型。建立离体大鼠31℃低温全心缺血55min,常温再灌注60min损伤模型。SD离体大鼠心脏随机分为4组(n=10/组):对照组(CON)用K-H液灌注50min后31℃低温缺血55min,常温复灌60min。异氟烷预处理组(ISC1、ISC2、ISC3),分别在缺血前给予0.5%、1.0%、2.0%的异氟烷预充饱和的K-H液灌注15min及洗脱15min。再灌注末,立刻分离心肌线粒体。观察指标有:LVEDP、LVSP、dp/dtmin、dp/dtmax、HR、梗死面积、线粒体和胞浆的细胞色素C。结果同对照组相比,复灌30min及60min时,各组LVSP、dp/dtmin、dp/dtmax、HR均无显著差异,仅ISC3组的LVDEP显著低于CON组(P<0·05)。复灌60min后ISC2组和ISC3组梗死面积显著低于CON组和ISC1组(P<0·05)。异氟烷预处理使浅低温缺血再灌注后心肌线粒体细胞色素C的释放减少。与CON组相比ISC3组胞浆细胞色素C的量明显减少(P<0·05),同时伴随线粒体的细胞色素C显著增加(P<0·05),ISC2组线粒体细胞色素C的量也显著多于CON组(P<0·05)。结论异氟烷预处理能通过诱导线粒体耐受(以线粒体细胞色素C丢失为线粒体功能障碍指标)抗心肌浅低温缺血再灌注损伤。Objective To investigate if isoflurane preconditioning is able to induce mitochondrial tolerance. Methods Hearts of SD rats was randomly assigned to a nontreated hypothermic ischemia group(CON) and three groups(ISC) respectively given 0.5%, 1.0% and 2.0% isoflurane 15 min with 15 min washout before 55 min hypothermic ischemia. Heart mitochondria was isolated after 60 min reperfusion. Hemodynamics, infarct size, cytosolic and mitochondrial cytochrome c were measured. Results Compared with the CON group, isoflurane exposure caused a reversible decrease in haemodynamic function in a concentration-dependent manner, but after reperfusion no differences between groups were observed except for diastolic left ventricular pressure(LVEDP). In ISC3 isoflurane preconditioning hearts exhibited a lower elevation of LVEDP compared with untreated ischemic control hearts after 15 min of reperfusion. Results showed isoflurane-preconditioning markedly reduced loss of mitochondrial cytochome c after reperfusion. Effects of 2.0% isoflurane on infarct size and cytochrome c release are more pronounced.Conclusion Regarding that isoflurane-preconditioning protected against myocardial damage resulting from moderate hypothermic ischemia, the results indicated that mitochondrial dysfunction may play an important role in isoflurane-preconditioning.

关 键 词：心肌线粒体 异氟烷 预处理 浅低温 线粒体细胞色素C dp/dtmin 耐受性 缺血再灌注损伤 线粒体功能障碍 离体大鼠心脏 梗死面积 LVEDP CON 灌注模型 离体心脏 SD大鼠 全心缺血 损伤模型 低温缺血 观察指标 LVSP 对照组 复灌 

分 类 号：R965[医药卫生—药理学]