ATP-MgCl2对缺血再灌注损伤大鼠心肌细胞一氧化氮合成酶的影响

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—MgCh组，而对照组cNOS活性则显著低于ATP—MgCh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。

Effect of ATP-MgCl2 on nitric oxide synthase during myocardial ischemia-reperfusion injury in rat

[Objective] To seek the relationship between myocardial ischemia-reperfusion injury and nitric oxide, and evaluate the mechanism of ATP-MgCl2 on myocardium after ischemia-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),respectively. The myocardial ischemia was induced by ceasing perfusion 30 min after heart was perfused at 10min on Langendorff device. The cNOS and iNOS activity were detected with Knowles method. [Results] The iNOS activity of the control group was remarkably higher than the cNOS activity of the ATP-MgCl2 group, and the cNOS 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.