无创性延迟肢体缺血预适应保护糖尿病大鼠缺血／再灌注心肌

目的：研究无创性肢体缺血预适应（NDLIP）对糖尿病（DM）大鼠心肌缺血／再灌注（I／R）损伤的影响。方法：大鼠经尾静脉一次性注射链脲佐菌素（STZ）造成急性DM模型后，被随机分为I／R、心脏缺血预适应（CIP）和NDLIP三组。NDLIP组连续3d经历左后肢缺血预适应。第4天，各组动物均经历I／R损伤，CIP组于缺血前行心肌缺血预适应。连续监测血压和心电图变化，观察NDLIP对DM大鼠I／R损伤后心肌电生理功能、心肌梗死范围和心肌酶学的影响，并测定心肌组织中超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH—Px）活性及丙二醛（MDA）含量。结果：成模动物表现出血糖明显升高，体重下降（P〈0．01）。与I／R组比较，NDLIP及CIP组ST一段抬高幅度降低，室早和室速出现时间推迟，持续时间缩短，室性心律失常发生率降低（P〈0．05），心肌梗死范围缩小（P〈0．01），心肌细胞乳酸脱氢酶（LDH）、肌酸激酶（CK）及其同工酶（CK—MB）的释放减少（P〈0．05，P〈0．01），心肌SOD、GSH—Px活性升高（P〈0．01），MDA含量减少（P〈0．05，P〈0．01）。结论：NDLIP可减轻DM大鼠I／R后心肌细胞损伤，从而减少心肌酶漏出、改善心脏生理功能，具有与CIP程度相当的心脏保护作用，其机制与调节心肌氧化．抗氧化系统功能平衡有关。

Cardiac protective effects of noninvasive delayed limb ischemic preconditioning against ischemia-reperfusion injury in diabetic rats

AIM: To study the effects of noninvasive delayed limb ischemic preconditioning (NDLIP) on myocardium ischemia-reperfusion injury in diabetic rats. METHODS: The acute diabetic rat models were induced by injecting streptozotocin (STZ) through vena caudalis. The diabetic rats were randomly divided into ischemia-reperfusion (I/R) group, cardiac ischemic preconditioning (CIP) group and NDLIP group. Rats in NDLIP group subjected to NDLIP left hind limb for 3 days, and at the fourth day, all rats were subjected to myocardial ischemia/reperfusion injury. Rats in CIP group were myocardial ischemic preconditioning before ischemia. Blood pressure and electrocardiogram were monitored continuously. The effects of myocardial electrophysiology function, myocardial infarction size and myocardial enzyme were observed in the diabetic rats with NDLIP after myocardium ischemia-reperfusion injury, and the superoxide dismutase(SOD), the activities of glutathion peroxidase(GSH-Px), the content of mal-onaldehyde in rats muscular tissues were detected. RESULTS: The levels of blood glucose were increased and the body weights were decreased in diabetic model rats(P < 0.01). Compared with I/R group, the elevation extent of ST segment in NDLIP and CIP group were degraded, the emergence time of ventricular premature contraction and ventricular tachycardia were delayed and the duration of both was shortened, and the incidence of ventricular arrhythmia was decreased (P < 0.05), the myocardial infarct size was reduced(P < 0.01), the releases of cadiocyte lactate dehydrogenase (LDH), creatine kinase (CK), and creatine kinase isozyme were decreased (P<0.05, P < 0.01), the activities of SOD and GSH-Px in rats muscular tissues were increased (P < 0.01) and the content of MDA was decreased in CIP and NDLIP groups(P < 0.05, P <0.01). CONCLUSION: NDLIP can relieve cadiocyte damage induced by I/R injury in the diabetic rats and the leakage of cardiac muscle enzyme is decreased, and the physiologic function of heart is improved, the cardiac protective effects of NDLIP group and CIP group are considerable. The effects are associated with the regulation of the equilibrium between oxidation and antioxidation system in myocardium.