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卡托普利心脏停搏液对缺血再灌注心肌NOS活性和NO产生的影响
引用本文:黄忠耀,朱洪生,张有荣,吴学军. 卡托普利心脏停搏液对缺血再灌注心肌NOS活性和NO产生的影响[J]. 中华胸心血管外科杂志, 1999, 15(3)
作者姓名:黄忠耀  朱洪生  张有荣  吴学军
作者单位:上海第二医科大学附属仁济医院心外科,200001
摘    要:目的:探讨卡托普利心脏停搏液对缺血再灌注心肌保护作用的机制。方法:12只绵羊,随机均分为对照组(I组)和卡托普利组(I组)。常规建立体外循环,心脏停搏60分钟,再灌注30分钟。I组采用仁济医院冷晶体停搏液,II组在停搏液中加入卡托普利23μmol/L。观察冠状窦血中一氧化氮(NO)、肌酸磷酸激酶(CPK)、环磷酸鸟苷(cGMP)、心肌丙二醛(MDA)含量及心肌NO合酶(NOS)同功酶活性的变化,监测心肌功能。结果:再灌注后I组心肌血NO、CPK、cGMP、心肌MDA均明显升高,I组低于I组(P<0.05或0.01)。II组再灌注后心肌原生型NO合酶(cNOS)活性明显高于I组,而诱导型NO合酶(iNOS)及总NOS活性显著低于I组(P<0.01或0.001)。两组再灌注后心肌功能均降低,I组较I组更为显著。再灌注后NO的变化与心肌MDA和CPK之间呈正相关(P<0.001和0.01)。结论:缺血再灌注心肌损伤与过量NO产生有关,卡托普利通过调节NOS同功酶活性,维持正常NO水平起到保护作用。

关 键 词:卡托普利  心肌  缺血再灌注  一氧化氮

The Protective Effect of Captopril-enriched Cardioplegic Solution on Myocardial NOS Activity and NO Prodution after InchemicReperfusion
HUANG Zhongyao,ZHU Hongsheng,ZHANG Yourong,et al.. The Protective Effect of Captopril-enriched Cardioplegic Solution on Myocardial NOS Activity and NO Prodution after InchemicReperfusion[J]. Chinese Journal of Thoracic and Cardiovascular Surgery, 1999, 15(3)
Authors:HUANG Zhongyao  ZHU Hongsheng  ZHANG Yourong  et al.
Affiliation:HUANG Zhongyao,ZHU Hongsheng,ZHANG Yourong,et al.Department of Cardiothoracic Surgery,Renji Hospital,Shanghai 200001
Abstract:Aim:This study was conducted to evaluate the protective effects of captoprilenriched cardioplegic solution on myocardial nitric oxide synthesis (NOS) and nitric oxide(NO) production after ischemic reperfusion.Method:The study consisted two groups of sheep.Group I(n=6) received cold crystalloid cardioplegia.Group II(n=6) received cardioplegia as same as group I but added captopril 23 mol/L.Blood samples were taken from coronary sinue at three different time intervals for assess following parameters:NO,CPK,cGMP.Myocardial specimens were also taken for MDA,iNOS,cNOS and NOS activities.Assessment of heart function including MAP,LVSP,LVEDP and dp/dtmax were performed at the same time intervals.Results:Plasma levels of NO,CPK,cGMP and myocardial MDA were increased significantly in group I after reperfusion 5 minutes and 30 minutes as compared with group II.cNOS activity was increased and iNOS and NOS activities were decreased significantly in group II.The heart function was compromised in both groups.There was a positive correlation between the change of NO and myocardial MDA and CPK.Conclusion:The excessive production of NO during reperfusion may be related to myocardial ischemic reperfusion injury.Captoprilenriched cardioplegia offers better myocardial protection effects than cold crystalloid cardioplegia alone.The protective effect may attributed to its effect of maintaining normal NO level through reducing iNOS activity and increasing cNOS activity.
Keywords:CaptoprilMyocardial protectionIschemiaReperfusionNitric oxide  
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