肺缺血后适应对兔急性心肌缺血再灌注损伤的作用

目的通过在体兔心肌缺血再灌注模型，探讨肺缺血后适应是否具有减轻心肌缺血再灌注（I／R）损伤的作用及其可能的作用机制。方法将30只兔随机分成3组，每组10只。对照组：结扎冠状动脉左前降支（LAD）30min，再灌注3h。缺血后适应组：结扎LAD20min时阻断左肺动脉5min，然后松开5min，继而心肌再灌注至3h。药物＋缺血后适应组：于结扎LAD25min后经耳缘静脉注射一氧化氮合酶（eNOS）抑制剂L-NAME10mg／kg，余同缺血后适应组。分别于缺血前、再灌注开始前、再灌注3h末取兔血，测定各组血清肌酸激酶（CK）、丙二醛（MDA）、及超氧化物歧化酶（SOD）的水平。结果再灌注3h末，CK活性后适应组低于对照组和药物＋缺血后适应组，MDA活性后适应组低于对照组和药物＋后适应组，SOD活性后适应组高于对照组和药物＋后适应组。药物＋后适应组与对照组比较，CK活性、MDA活性和SOD活性均无统计学意义。结论肺缺血后适应对急性心肌缺血再灌注损伤具有保护作用；减少氧自由基的产生和释放NO是肺缺血后适应的作用机制。

Protective Effect of Lung Ischemic Postcondition on Cardiac Ischemic Reperfusion

Objective To explore the protective effect of lung ischemic postconditioning on rabbit cardiac ischemic-reperfusion model in vivo.Methods Thirty rabbits were randomized to one of three groups;Control:LADO 30 min and 3 h reperfusion;IPC:after 20 minutes of LADO,the left pulmonary was occluded for 5 minutes and released 5 minutes before coronary artery reperfusion;Drug IPC:after LADO 25 minutes,rabbit received 10 mg/kg L-NAME,the other steps follow IPC.Blood CK,MDA and SOD were measured before ischemic,before reperfusion and at the time of 3 hour reperfusion.Results After 3 hours reperfusion the levels of CK and MDA were lower and SOD were higher in group IPC than that in other groups,there were no differences about all indexes between group L-NAME and control.Conclusion Pulmonary ischemic postconditioning could play protective role in myocardium from reperfusion injuries,which might be related to decreasing free radical and releasing NO.