摘要
观察心肌局部肾素－血管紧张素系统（ＲＡＳ）在心肌缺血再灌注损伤时的激活情况及特异性非肽类血管紧张素Ⅱ１型受体（ＡＴ１）阻断剂Ｌｏｓａｒｔａｎ的保护效应。方法离体大鼠心脏灌流模型，心功能测定，放射免疫测定。结果心肌缺血４０ｍｉｎ后，心肌内ＡｎｇⅡ即明显增高（Ｐ＜０．０１），ＡｎｇⅠ增高尚不明显；再灌１０ｍｉｎ后，ＡｎｇⅠ、ＡｎｇⅡ均明显升高（Ｐ＜０．０１），Ｌｏｓａｒｔａｎ５μｍｏｌ／Ｌ不明显影响这种增高，但却能使缺血再灌注损伤后的心功能得到明显改善，减少心肌肌酸激酶（ＣＫ）的释放。结论一定时间的缺血和再灌注均能使心肌组织中ＲＡＳ有所激活，ＡｎｇⅡ增高可加重缺血心肌的损伤。
AimToinvestigatetheactivationofintracardiacrenin-angiotensinsystem(RAS)duringischemiaandreperfusioninisolatedperfusedratheartsandthecardioprotectiveefectoflosartan,theangiotensinⅡ(AngⅡ)type1receptorantagonist.MethodsIsolatedperfusedrathearttechniquesinfourtyWistarrats(dividedintofourgroup:control,is-chemia,ischemiaandreperfusiongroupandreperfu-siontreatedwithlosartangroup);heartfunctionmeasuredbyHR,LVDP,LVEDPanddp/dtmax;weredeterminedbyradioimmumoassayAngⅠandAngⅡ.ResultsImmunoreactiveAngⅡofthehearttissueswaselevatedsignificantly(P<0.01vscontrol)butAngⅠelevationfailedtoreachsignifi-canceafter40minglobalischemia.However,AngⅡandAngⅠwerebothincreasedtoasignificantextent(P<0.01vscontrol)folowing10minreperfusion.Losartan(5μmol)improvedtherecoveryofcardiacfunctionanddecreasedreperfusioncreatinekinase(CK)releasewithoutmarkedinfluenceonthein-creasedAngⅡandAngⅠlevelsofthehearttissues.ConclusionThesedataindicatedthatischemiaandreperfusionaremorelikelytobeacauseoftheactivationtolocalcardiacRAS.IncreasedAngⅡmaycontributetotheinjuryofischemicmyocardium.ThebeneficialefectoflartanisprobablyascribedtotheblockadeofspecificAngⅡreceptor.
出处
《高血压杂志》
CSCD
1996年第3期178-181,共4页
Chinese Journal of Hypertension
基金
国家"八五"攻关资助课题
关键词
心脏
血管紧张素
缺血再灌注
心功能
RAS
ratheartlocalrenin-angiotensinsystemischemiaandreperfusioncardiacfunctionlosartan
