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目的观察无创性延迟肢体缺血预适应(NDLIP)对糖尿病大鼠心肌缺血再灌注损伤的保护作用,并探讨氧化-抗氧化对其的作用机制。方法尾静脉注射链脲佐菌素(STZ)制备糖尿病大鼠模型。将糖尿病大鼠随机分成心肌缺血再灌注(I/R)、早期心肌缺血预适应(EMIP)和无创性延迟肢体缺血预适应(NDLIP)组。NDLIP组连续3d经历左后肢缺血预适应。第4d,各组动物均经历心肌I/R程序,EMIP组于缺血前行心肌缺血预适应,连续监测心电图变化,检测心肌梗死范围,测定心肌组织中丙二醛(MDA)含量、总-超氧化物歧化酶(T-SOD)、锰-超氧化物歧化酶(Mn-SOD)活力及Mn-SOD mRNA表达情况。结果与I/R组相比,EMIP组和NDLIP组ST-段抬高幅度降低,室早出现时间明显推迟,持续时间明显缩短,室速和室颤发生率均明显降低,心肌组织梗死范围明显缩小,MDA含量明显下降,而T-SOD、Mn-SOD活力明显升高及Mn-SOD mRNA表达量增加。结论无创性延迟肢体缺血预适应可以增强糖尿病大鼠的心肌抗氧化能力。
Objective To observe the protective effect of noninvasive delayed limb ischemic preconditioning (NDLIP) on myocardial ischemia-reperfusion injury in diabetic rats and to explore the mechanism of its action. Methods Diabetic rats were induced by injecting streptozotocin (STZ) into tail vein. The diabetic rats were randomly divided into myocardial ischemia reperfusion (I / R), early myocardial ischemic preconditioning (EMIP) and noninvasive delayed limb ischemic preconditioning (NDLIP) group. The NDLIP group was subjected to ischemic preconditioning of the left hind limb for three consecutive days. On the 4th day, the myocardial I / R programs were observed in all groups. EMIP group was subjected to ischemic preconditioning, the changes of electrocardiogram were monitored continuously, the extent of myocardial infarction was detected, the content of malondialdehyde (MDA) The activity of superoxide dismutase (T-SOD), manganese-superoxide dismutase (Mn-SOD) and the expression of Mn-SOD mRNA. Results Compared with the I / R group, the amplitude of ST-segment elevation in EMIP group and NDLIP group was significantly lower than that in the I / R group (P <0.05). The early onset time was significantly delayed, the duration was significantly shortened, the incidence of ventricular tachycardia and ventricular fibrillation were significantly decreased, , MDA content decreased significantly, while T-SOD, Mn-SOD activity was significantly increased and Mn-SOD mRNA expression increased. Conclusion Noninvasive delayed limb ischemic preconditioning can enhance myocardial antioxidant capacity in diabetic rats.