中文摘要：

目的：研究无创性延迟肢体缺血预适应（noninvasive delayed limb ischemic preconditioning，NDLIP）对脑缺血再灌注大鼠内皮细胞分泌功能的影响并探讨其作用机制。方法：健康雄性Wistar大鼠随机分为假手术组（Sham）、脑缺血再灌损伤（ischemia-reperfusion injury, I/R）组、早期脑缺血预适应（early cerebral ischemic preconditioning，ECIP）组和NDLIP组，建立大鼠脑缺血再灌注模型，实施1 h缺血/24 h再灌注，ECIP组于缺血前左侧颈总动脉行3次5 min缺血/5 min再灌注，NDLIP组于缺血前3天每天左后肢实施3次5 min缺血/5 min再灌注。TTC染色法测定脑梗死面积，分别在缺血前及再灌注24 h后测定血清内皮素（endothelin, ET-1）、一氧化氮（nitric oxide, NO）的含量及组织纤溶酶原激活物（tissue plasminogen activator, t-PA）、纤溶酶原激活物抑制剂（plasminogen activator inhibitor, PAI-1）的活力。结果：缺血前，与I/R组比较，ECIP组和NDLIP组血清NO浓度升高（P〈0.05），ET-1/NO比值降低（P〈0.05），再灌注后，与I/R组比较，ECIP组和NDLIP组梗死范围显著减小，血清ET-1降低（P〈0.01），NO增加（P〈0.01），ET-1/NO比值降低（P〈0.05），t-PA活力升高（P〈0.01），PAI-1活力降低（P〈0.01）。结论：NDLIP可能是通过调整内皮细胞分泌收缩与舒张、促凝与抗凝物质的平衡，起到抵抗脑缺血再灌注损伤的作用，并且其保护程度与ECIP相当。

英文摘要：

OBJECrlVE To investigate effects of noninvasive delayed limb ischemic preconditioning （NDLIP） on secretive functions of vascular endothelial cells in rats with cerebral ischemia-reperfusion injury. METHODS Healthy male Wistar rats were divided randomly into operation group, cerebral ischemia-reperfusion （I/R） group, early cerebral ischemic preconditioning （ECIP） group and noninvasive delayed limb ischemic preconditioning （NDLIP） group. The model of cerebral I/R was estab- lished by 1 h of occlusion of middle cerebral artery followed by 24 h of reperfusion. Rats in ECIP group were subjected to 3 cy- cles of 5 rain of ischemia and reperfusion on common carotid artery before 1 h of ischemia and 24 h of reperfusion. Rats in NDLIP group were subjected to 3 cycles of 5 min of ischemia and reperfusion on left hind limb for 3 days to induce NDLIP. On the forth day, 1 h of ischemia and 24 h of reperfusion was performed. Cerebral infarction size was determined 24 h after I/R by TTC staining. Contents of nitric oxide （NO）, endothelin （ET-1）, tissue plasminogen activator （t-PA） and plasminogen activa- tor inhibitor （PAI-1） were measured before ischemia and 24 h after reperfusion, respectively. RESULITS Under normal condi- tions, NDLIP increased NO concentration in serum, slanted the balance between ET-I and NO toward NO. After I/R injury, infarction sizes of ECIP and NDLIP group decreased. NDLIP decreased the disturbance of endothelial function, increased NO in serum, decreased ET-1 concentration and maintained the balance between ET-1 and NO to approach normal. NDLIP increased t-PA activities and decreased PAI-1 activities. CONCLUSION NDLIP can protect brain from ischemia-reperfusion injury, which may contribute to its action on regulating the balance between vascular dilatation and contraction, procoagulant and anti- coagulant substances secreted by vascular endothelial cells. The protective effects of NDLIP were equivalent to those of ECIP.