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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 d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,抵抗脑缺血再灌注损伤的作用,其保护程度与ECIP相当。
Objective: To investigate the effect of noninvasive delayed limb ischemic preconditioning (NDLIP) on the secretion of endothelial cells in rats with cerebral ischemia-reperfusion injury and to explore its mechanism. Methods: Healthy male Wistar rats were randomly divided into sham operation group, ischemia-reperfusion injury (I / R) group, early cerebral ischemic preconditioning (ECIP) group And NDLIP group, the model of cerebral ischemia / reperfusion in rats was established. The ischemia / reperfusion was performed at 1 hour and 24 hours after reperfusion. The left common carotid artery in the ECIP group was reperfused three times for 5 min ischemia / 5 min. Group 3 days before ischemia 3 h left hind limbs 5 min ischemia / 5 min reperfusion. TTC staining was used to measure the area of cerebral infarction. The levels of endothelin (ET-1), nitric oxide (NO) and tissue plasminogen activator (tissue plasminogen activator, t-PA) and plasminogen activator inhibitor (PAI-1). Results: Compared with I / R group, serum NO level in ECIP group and NDLIP group increased (P <0.05) and ET-1 / NO ratio decreased (P <0.01), NO increased (P <0.01), ET-1 / NO decreased (P <0.05), and t-PA activity in ECIP group and NDLIP group decreased significantly (P <0.01), the activity of PAI-1 decreased (P <0.01). Conclusion: NDLIP may protect endothelial cells against ischemia-reperfusion injury by regulating the balance between contraction and relaxation of endothelial cells and the balance between procoagulant and anticoagulant substances.