ATP-MgCl_2对缺血再灌注损伤大鼠心肌细胞一氧化氮合成酶的影响  

Effect of ATP-MgCl_2 on nitric oxide synthase during myocardial ischemia-reperfusion injury in rat

作　　者：车成日[1] 金虎日[1] 林承平[1] 

机构地区：[1]延边大学医学院附属医院胸心外科,吉林延边133000

出　　处：《中国现代医学杂志》2005年第20期3118-3119,共2页China Journal of Modern Medicine

摘　　要：目的寻找心肌缺血再灌注损伤与一氧化氮(NO)的关系,进一步探讨高能磷酸盐制剂ATP-MgCl2对缺血再灌注大鼠心肌保护作用的机制。方法选用健康SD大鼠16只,随机分为两组(n=8),开胸取心,在Langgendorff灌流装置上进行主动脉灌注10min,待心肌收缩稳定后,停止灌流30min,再分别以相应灌注液灌注20min,对照组:使用Krebs-Henseleit(KH)缓冲液;ATP-MgCl2组:使用KH缓冲液+ATP-MgCl2(0.1mmol/L)。以Knowles方法测定心肌原生型NOS(cNOS)和诱导性NOS(iNOS)活性。结果对照组iNOS活性显著高于ATP-MgCl2组,而对照组cNOS活性则显著低于ATP-MgCl2组。结论ATP-MgCl2通过减少因iNOS所产生的氧自由基浓度而起到心肌保护作用。[Objective] To seek the relationship between myocardial ischemia-reperfusion injury and nitric oxide, and evaluate the mechanism of ATP-MgCl2 on myocardium after isehemia-reperfusion in Rat. [Methods] Sixty SD rats were randomly divided into two groups： Control group and ATP-MgCl2. group reperfusion solution were Krebs-Henseleit（KH） buffer solution and KH buffer solution ＋ ATP-MgCl2 （0.1mmol/L）,respeetively. The myocardial ischemia was induced by ceasing perfusion 30 rain after heart was perfused at 10min on Langendorff device. The eNOS and iNOS activity were detected with Knowles method. [Results] The iNOS activity of the control group was remarkably higher than the eNOS activity of the ATP-MgCl2 group, and the eNOS activity of the control group was remarkably lower than the iNOS activity of the ATP-MgCl2 group. [Conclusions] The myocardial protection mechanism of ATP-MgCl2 maybe be attributed to reduced oxygen free radical concentration induced by iNOS.

关 键 词：ATP—MgCl2 缺血再灌注损伤心肌 一氧化氮合成酶 

分 类 号：R969[医药卫生—药理学]