中文摘要：

目的探讨无创肢体缺血预适应对大鼠心肌缺血／再灌注损伤的保护作用及机制。方法56只健康6Wistar大鼠随机分为缺血／再灌注（I／R）组、肢体缺血预适应（LIP）组、I／R＋5-羟基癸酸钠（5-hydroxydecanoate，5-HD）组和LIP＋5-HD组。LIP组和LIP＋5-HD组左后肢每天经历3次5min缺血／5min再灌注，连续3d。d4，全部大鼠冠状动脉左前降支经历30min缺血／120min再灌注，I／R＋5-HD组和LIP＋5-HD组于缺血前及I／R期间给予mitoKATP阻断剂5-HD。测定心肌梗死面积、心肌细胞凋亡指数、凝血酶原时间、活化部分凝血活酶时间和纤维蛋白原含量，观察心肌形态学改变。结果与I／R组相比，LIP能缩小心肌梗死面积（约38．24％，P〈0．05），减少心肌细胞凋亡（约23．33％，P〈0．01），改善心肌形态学改变。LIP对基础状态下的凝血功能无影响，但能降低I／R后血浆纤维蛋白原增加程度（约12．5％，P〈0．05）。上述LIP作用被5-HD取消。结论LIP对大鼠心肌I／R损伤具有保护作用，机制可能涉及mitoKATP的开放。

英文摘要：

Aim To explore the protection of noninvasive limb ischemic preconditioning （LIP） against myocardial ischemic reperfusion （I/R） injury in rats and its mechanism. Methods 56 healthy male Wistar rats were divided randomly into I/R, LIP, I/R ＋ 5-hydroxy- decanoate （5-HD） and LIP ＋ 5-HD groups. Rats in LIP and LIP ＋ 5-HD groups were subjected to 3 cycles of 5 rain ischemia and reperfusion on the left hind limb for 3 days to induce LIP. On the fourth day, all rats were subjected to 30 rain ischemia of the left coronary artery anterior descending （LAD） followed by 120 rain of reperfusion. Rats in I/R ＋ 5-HD group and LIP ＋ 5- HD group were given 5-HD, a special blocker of mitochondrial ATP-sensitive potassium channel before ischemia and during the period of ischemia and reperfusion. Myocardial infarct size, cadiocyte apoptosis index, prothrombin time, activated partial thromboplastin time, fibrinogen were measured. Changes of myocardial morphology were observed. Results Compared with I/R group, LIP decreased myocardial infarct size （ about 38.24%, P 〈 0. 05 ） and cell apoptosis （about 23.33%, P 〈 0. O1 ）, attenuated myocardial morphological injury. LIP had no effect on coagulation in normal condition, but it decreased the extent of plasma FIB increase after I/R injury（ about 12.5% ,P 〈0.05）. The protective effects induced by LIP were canceled by 5-HD. Conclusion LIP can protect against myocardial ischemia reperfusion injury, which may be related to the opening of mitochondrial ATP- sensitive potassium channel.