一氧化氮在大鼠心肌缺血后处理中的作用

目的:探讨在体条件下,一氧化氮(NO)对缺血后处理心肌保护作用的影响及可能的途径。方法:建立大鼠在体缺血再灌注模型,将24只大鼠随机分为假手术组、缺血再灌注组、缺血后处理组及一氧化氮合酶(NO S)抑制剂NW-L硝-基精氨酸甲酯(L-NAM E)药物干预后处理组(药物干预组)。于再灌注末测定血浆肌钙蛋白I(cT n I),NO,超氧化物歧化酶(SOD)及丙二醛(M DA)的含量,测定心肌组织梗死面积,免疫组化方法观察心肌组织内皮型一氧化氮合酶(eNO S)的表达。结果:与缺血再灌注组及药物干预组相比,缺血后处理组心肌梗死面积明显减少,血浆cT n I,M DA含量降低,血浆NO,SOD含量升高,心肌细胞胞浆内eNO S表达增加。结论:缺血后处理通过eNO S/NO信号通路,抑制脂质过氧化反应,减轻心肌缺血/再灌注损伤。

Effects of nitric oxide on ischemic postconditioning in rat hearts

Objective:To investigate the effection of nitric oxide(NO)on ischemic postconditioning and the possible protective mechanisms.Methods:Twenty-four wistar rats were randomly divided into five groups:sham operated group,ischemia-reperfusion group,ischemic postconditioning group,nitric oxide synthase(NOS)inhibitor NW-L-Nitro arginine methyl ester(L-NAME)group(drug intervention group).Cardiac treponin I(cTnI),nitric oxide(NO),malonaldehyde(MDA),superoxide dismutase(SOD)in plasma were tested after ischemia reperfusion.Myocardial infarct size was measured by image analytical system.The expression of eNOS in myocardial tissue was investigated by immunohistochmistry.Results:Infarct size was significantly increased in ischemic postconditioning groupcompared with ischemia-reperfusion group and drug intervention group.The concentration of cTnI,MDA in plasma were comparably reduced,the concentration of NO and SOD in plasma were obviously rised,the expression of eNOS was incresed in ischemic postconditioning group.Conclusion:NO and eNOS play a role in the protection of ischemic postconditioning,ischemic postconditioning protects the heart against ischemia-reperfusion injury by the reduction of the injury of free radicals.