中文摘要：

目的：观察大鼠心肌缺血后适应（IPost）对血清细胞因子的影响,探讨内皮型一氧化氮合酶的作用及其机制。方法：50只SD雄性大鼠随机分为5组：假手术组（A组）、缺血再灌注（I/R）组（B组）、IPost组（C组）、左旋硝基精氨苯甲酯（L.NAME）＋I/R组（D组）和L.NAME＋IPost组（E组）。结扎冠状动脉左前降支建立I/R损伤模型,除A组外,其余各组均行缺血30 min、再灌注2 h;C组和E组分别在缺血30 min后立即给予3个循环的10 s再灌注和10 s缺血;D组和E组在缺血前再给予L.NAME。再灌注15 min、30 min、1 h、2 h时取血,测定白细胞介素（IL）-6和IL-10水平;再灌注2 h取血后处死大鼠,计算梗死面积占横切面的百分比。结果：①C组大鼠心肌梗死面积占横切面的百分比小于B组（P〈0.05）,E组大于C组（P〈0.05）,而D组与B组之间差异无统计学意义（P〉0.05）;②与B组比较,C组IL-6水平较低,IL-10水平较高;③与C组比较,E组IL-6水平升高,IL-10水平降低;④B组与D组IL-6和IL-10水平比较差异均无统计学意义。结论：IPost能降低促炎细胞因子（IL-6）、升高抗炎细胞因子（IL-10）水平,其机制可能与内皮型一氧化氮合酶参与炎症因子的调节有关。

英文摘要：

Objective：To determine whether ischemic postconditioning（IPost）could affect the level of inflammatory cytokines and the role of endothelial nitric oxide synthase in this phenomenon.Method：Male SD rats（n=50） were randomly divided into five groups,including sham group,ischaemia/reperfusion（I/R） group,IPost group,L.NAME-treated before postconditiong（L.NAME＋IPost） group and L.NAME-treated before I/R（L.NAME＋I/R） group.In this process,blood was drawn to assay serum IL-6 and IL-10 levels at 15 min,half an hour,one hour and two hour after reperfusion.Rats were killed for measuring myocardial infarct size.Result：IPost reduced the infarct size（P0.05）,and this protection disappeared when L.NAME was given before I/R.IPost could reduce the serum level of IL-6 and increase the level of IL-10 in the IPost group compared with those in the I/R group（P0.05）,but such changes had not shown when L.NAME was given beforeI/R.There was no significant difference of IL-10 and IL-6 levels between the I/R group and L.NAME＋I/R group（P0.05）.Conclusion：The protective effect of ischemic postconditioning may be retated to decrease of proinflammatory cytokine level and increase of anti-inflammatory cytokine level which are modulated by enhancement of endothelial nitric oxide synthase activity.