一氧化氮在大鼠模拟心肌缺血/再灌注损伤中的作用

目的探讨一氧化氮(NO)在大鼠心肌缺血/再灌注损伤(IRI)中的作用。方法20只Wistar雄性大鼠随机分成假手术组,缺血30min再灌注180min组(IRI组)。检测:①心肌组织及血清中NO2-+NO3-值;②心功能指标:心率(HR)和平均动脉压(MAP);③血清肌酸激酶同工酶(CK-MB)含量;④以缺口末端标记法(TUNEL)检测心肌细胞凋亡的变化。结果心肌细胞缺血再灌注后:①心肌组织NO2-+NO3-IRI组较假手术组增高26.7%(P<0.05),血清NO2-+NO3-IRI组较实验后较实验前升高41.1%(P<0.01);②HR和MAPIRI组显著低于假手术组;③血清CK-MB含量IRI组较假手术组升高51%(P<0.01);④心肌组织TUNEL染色IRI组检测到大量阳性凋亡细胞,凋亡细胞阳性指数(AI)IRI组较假手术组升高89.4%(P<0.01)。结论NO升高可能是诱导细胞凋亡,加重心肌细胞缺血/再灌注损伤的重要原因之一。

The role of nitric oxide in rat myocardial ischemic-reperfusion injury

Objective To study the role of nitric oxide(NO) in myocardial ischemia reperfusion injury(IRI) in rat models.Methods Twenty Wistar male rats were randomized into two groups:the Sham-group and IRI group.IRI model was produced by 30-min ischemia and 180-min reperfusion.Contents of NO2- NO3-in myocardium homogenate and in serum,serum level of creatine kinase isoenzyme MB(CK-MB) were determined,cardiac functional indices(heart rate [HR] and mean artery pressure [MAP]) were recorded,and cardiomyocyte apoptosis was examined by TUNEL techniques.Results Compared with the Sham group,IRI group showed:(1) increases in myocardial NO2- NO3-by 26.7%(P<0.05) and in serum level of NO2- NO3-by 41.1%(P<0.01);(2) significantly lowered HR and MAP;(3) elevation in the level of CK-MB by 51%(P<0.01);(4) a large number of apoptotic cardiomyocytes,leading to a rise in apoptosis index(AI) as much as 89.4%(P<0.01).Conclusion The higher level of NO might be one of important factors contributive to induction of myocardial apoptosis and deteriorated progression of IRI.