激活k阿片受体与远程预处理诱导心肌缺血耐受的作用的论文

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1、激活K阿片受体与远程预处理诱导心肌缺血耐受的作用的论文【摘要】目的：比较k阿片受体激动剂u50488h预处理与远程预处理诱导心肌缺血耐受对心肌梗塞（mi）范围与心肌酶的影响。方法：32只雄性新西兰大白兔随机分成四组（各组8例）：对照组、u50488h组、远程缺血预处理（rpc）组和选择性k阿片受体阻断剂（nor-bni）+u50488h组。对照组心肌缺血前1.5h静脉给予戊巴比妥钠30mg/kg；rpc组在心肌缺血前1.5h静脉给予戊巴比妥钠30mg/kg麻醉动物后，行双后肢短暂缺血预处理2次（充气式压力止血带环扎双后肢腘窝上1/3，压力26.6kpa，每次10min，间隔1

2、0min）；u50488h组在心肌缺血前105min静脉注射u50488h1.5mg/kg，余同rpc组；nor-bni+u50488h组在预处理前15min给予nor-bni2mg/kg，余同u50488h组。各组最后制作急性心肌缺血模型：冠状动脉左前降支完全闭塞45min，松开结扎圈再灌注2h。依据美蓝、ttc组织染色，观察各实验组mi质量比、肌钙蛋白t、心肌酶的变化。结果：u50488h可模拟rpc对心肌的保护作用，较对照组明显减少心肌缺血-再灌注损伤所致的mi［（0.15±0.11）g∶（0.29±0.11）g］，肌钙蛋白t［冠脉阻闭45min（3.86±1.19）n

3、g/ml∶（9.16±2.82）ng/ml］，心肌酶的含量，p均<0.01。该作用可被选择性k阿片受体阻断剂nor-bni所阻断。结论：rpc诱导心肌缺血耐受与k阿片受体激活具有密切关系，激活k阿片受体是rpc诱导心肌缺血耐受的机制之一。.【关键词】缺血预处理；心肌缺血；肌钙蛋白teffectofactivatedk-opioidreceptorandremotepreconditioningonmyocardiumischemiatoleranceentofanesthesiology,qigeneralhospital,lanzhoumilitarydistrict

4、,qi,xnjiang,830000,chinaabstract：objective:tostudytheeffectsofu50488h(aselectivekopioidreceptoragonist)onthesizeofmyocardialischemicreperfusionandtheplasmacontentsofmyocardiumenzymeparedoteischemicpreconditioningfrommyocardialischemiainrabbits.methods:atotalof32malenelydividedintofourgrou

5、ps:remotepreconditioninggroup(rpc),ischemiareperfusiongroup(control),u50488hgroupandkopioidreceptorblockingagent(nor-bni)+u50488hgrouprespectively.thedetailedexperimentalprotocolsalsincontrolgroupinbypentobarbitalsodium(sp)30mg/g,alsinrpcgroupg/gi.vandreceivedbothhindlimbischemiaprecondi

6、tioning2timesmhgfor10minininterval,thenfolloinreperfusion；inu50488hgroup，allanimalsg/gbeforemyocardialischemia,thenstepasrpcgroup.in(nor-bni)+u50488hgroupallanimalsg/kgbeforemyocardialischmemia，thenstepasu50488hgroup.themodelofmyocardialischmemiaadeintheendofeachgroup.leftanteriordescending

7、coronaryarteryinandfolloinedbystainingethyleneblueandtriphenyltetrazoliumchloride(ttc)respectively.results:paredtroponint［（9.16±2.82）ng/mlvs.（3.86±1.19）ng/ml］(p<0.01all)andmyocardiumenzymecausedbymyocardialischemiareperfusioninjury(p<0.05all),entan