一氧化氮合酶在缺血预适应诱导第二心肌保护窗口中的作用  

The role of nitric oxide synthase in development of the second window of protection in rabbits with ischemic preconditioning

作　　者：郑斌[1] 党瑜华[1] 陈魁[1] 

机构地区：[1]河南医科大学第一附属医院心内科,河南郑州450052

出　　处：《中国危重病急救医学》2001年第10期598-600,共3页Chinese Critical Care Medicine

基　　金：河南省科委科研基金资助项目 ( No.991 1 70 3 2 1)

摘　　要：目的 :探讨一氧化氮合酶在缺血预适应诱导第二心肌保护窗口减少心肌梗死范围中的作用。方法 :结扎冠状动脉复制心肌缺血预适应及心肌梗死模型。斑点印迹法测定心肌热休克蛋白 72含量。结果 :缺血预适应前静注一氧化氮合酶抑制剂 (左旋硝基精氨酸 )可使缺血预适应组的心肌梗死范围由 ( 2 2 .6± 5.9) %扩大至( 40 .1± 8.3 ) % ,与对照组 ( 44 .2± 8.1 ) %水平相似。亦可使缺血预适应诱导的心肌热休克蛋白 72表达由 3 .3±0 .8降至 2 .3± 0 .8,与对照组水平 1 .8± 0 .6相似。结论 :一氧化氮合酶在缺血预适应诱导第二心肌保护窗口过程中发挥重要作用。其作用可能与其参与诱导心肌热休克蛋白 72表达有关。Objective:To test the hypothesis that development of the second window of protection (SWOP) against myocardial infarction is triggered by nitric oxide synthase (NOS) in ischemic preconditioning (IPC).Methods:In an openchest rabbit model,IPC and myocardial infarction were achieved by coronary occlusions.The content of heat shock protein 72 (HSP72) in cardiac muscle was measured by dot blot analysis.Results:In phaseⅠ,N WnitroLarginie(LNA,NOS inhibitor) blocked the SWOP against myocardial infarction.LNA increased the infarct size in IPC group from (22 6±5 9)% to (40 1±8 3)%.In phaseⅡ,LNA abolished the expression of HSP72 induced by IPC.LNA decreased the HSP72 value in IPC group from 3 3±0 8 to 2 3±0 8.Conclusions:NOS plays an important role in the development of SWOP,which may be related to the expression of HSP72.

关 键 词：缺血预适应 一氧化氮 一氧化氮合酶 热休克蛋白 左旋硝基精氨酸 

分 类 号：R541.4[医药卫生—心血管疾病]