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大鼠心肌缺血再灌注损伤及中性粒细胞浸润与一氧化氮心肌保护作用的研究
引用本文:吴丹宁,贾国良,马颖艳,李伟.大鼠心肌缺血再灌注损伤及中性粒细胞浸润与一氧化氮心肌保护作用的研究[J].临床军医杂志,2003,31(4):1-4.
作者姓名:吴丹宁  贾国良  马颖艳  李伟
作者单位:1. 解放军第117医院,心内科,浙江,杭州,310013
2. 第四军医大学西京医院,心内科,陕西,西安,710032
摘    要:目的 中性粒细胞(Neu)心肌浸润是心肌缺血-再灌注(I/R)损伤的重要机制之一。本实验通过在SD大鼠中建立心肌I/R模型,研究I/R过程中心肌损伤与中性粒细胞浸润的关系,并通过左型精氨酸(L-Arg)干预,探讨一氧化氮(NO)对中性粒细胞浸润的影响及其在心肌I/R损伤中的保护作用。方法 实验分对照(CON)组、L-Arg处理组。每组又分缺血前、缺血40 min、再灌 1h、再灌 3h和再灌6 h 5个时间点,分别测定各组各时间点血清肌酸磷酸激酶(CPK)及心肌匀浆丙二醛(MDA)值,并观察心肌组织病理学的改变。结果 (1)CPK及心肌匀浆MDA测定结果:再灌注后各时相血清CPK及肌匀浆MDA含量较缺血前明显上升,再灌注3h后达到高峰。L-Arg组中再灌注后各时相点血清CPK及肌匀浆MDA明显低于CON组(P<0.05)。(2)H-E染色结果:缺血前心肌细胞完整,边界清楚,心肌横纹清晰。CON组:再灌后1h出现Neu心肌浸润,再灌3 h Neu心肌浸润更明显,累及心肌全层,伴有局灶心肌坏死;再灌6 h后Neu浸润尤甚,大片心肌坏死,并可见小血管内Neu聚集现象。L-Arg组:再灌注后Neu心肌浸润明显减少,再灌6 h心肌坏死灶较CON组明显缩小。结论 (1)心肌I/R过程中有大量Neu心肌浸润,与心肌损伤密切。(2)L-Arg能抑制Neu心肌浸润,具有心肌保护作用。

关 键 词:中性粒细胞  缺血—再灌注  一氧化氮  精氨酸  心肌保护
文章编号:1671-3826(2003)04-0001-04
修稿时间:2003年4月15日

The Experimental Study on the Role of Neutrophil Infiltration and the Myoardial Protection of the Nitric Oxide During Ischemia Reperfusion in Rats
Wu Dan-ning,Jia Guo-liang,Ma Yin-yan,La Wei.The Experimental Study on the Role of Neutrophil Infiltration and the Myoardial Protection of the Nitric Oxide During Ischemia Reperfusion in Rats[J].Clinical Journal of Medical Officer,2003,31(4):1-4.
Authors:Wu Dan-ning  Jia Guo-liang  Ma Yin-yan  La Wei
Abstract:Objective The neutrophil infiltration is one of the reasons which lead to the myocardial ischemic reperfusion (I/R) injury. The study aimed at investigating the changes between myocardic injury and neutrophil infiltration during I/R, and inquiring into the mechanisms of myocardial protection against I/R injury by intravenous infusion of L-arginine ( L-Arg) in ratty myocardial I/R model. Methods The rats were divided into 2 groups, including the Control and L-Arg infusion group, each with pre - ischemia , post-ischemia 40mins, reperfusion for 1h ,3 hrs and 6hrs subunits. The changes of serum CPK、myocardial MDA、 histopathology were examined . Results Result were showed that the levels of serum CPK and myocardial MDA increased after reperfusion, and reached the highest at 3hrs followed reperfusion, the content in the L-Arg groups were significantly lower(P <0.05 Vs CON) and that histopathologically the myocanlial neutrophil infiltration appeared at 1h followed reperfusion, and increased with the continue of the reperfusion , accompanied by the myocyte necrosis in the control group. With the L-Arg infusion intraveneously following ischemia , decrease of neutrophil infiltration and myocyte necrosis were showed in rats . Conclnsion (1) The myocardial neutrophil infi ltration indicates neutrophials participate in impairing the myocardium during I/R; (2)The L-Arg prevents the neutrophila irom my-ocardial infiltration , and ameliorate the ischemic - reperfuaion injury.
Keywords:neutrophill  ischemia reperfusion  nitric oxide  L-argnine  myocardium protection  
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