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.
出处
《中国现代医学杂志》
CAS
CSCD
北大核心
2005年第20期3118-3119,共2页
China Journal of Modern Medicine