中文摘要：

目的：研究缺血后处理（Ⅰ～postC）对脑缺血／再灌注（I／R）大鼠软脑膜微循环的改善作用及其机制。方法：32只雄性Wistar大鼠随机分为假手术（sham）、I／R、Ⅰ—postC及缺血预处理（IPC）组，采用颈动脉引流法建立大鼠全脑I／R损伤模型，于实验结束时观测软脑膜微循环和脑表面血流量变化，酶联免疫吸附法测定血浆可溶性细胞间黏附分子-1（sICAM-1）含量，试剂盒测定脑组织髓过氧化酶（MPO）、超氧化物歧化酶（SOD）活性及丙二醛（MDA）含量，免疫印记法检测脑组织血管内皮钙黏蛋白（VE—cadherin）和NF—KBp65的表达。结果：（1）Ⅰ—postC明显改善微循环血流状态，减轻I／R所致的细动静脉收缩和脑表面血流量降低（均P〈0．05），且脑组织VE—cadherin量减少程度较I／R组减轻（P〈0．05）；（2）与I／R组比较，I—postC组血浆sICAM-1含量、脑组织MPO活性和MDA含量降低（P〈0．05或P〈0．01），SOD活性增高（P〈0．05），且脑组织NF—KBp65表达下调（P〈0．05）。结论：Ⅰ—postC可改善脑I／R大鼠软脑膜微循环，其机制与抑制ICAM-1介导的中性粒细胞活化有关。

英文摘要：

AIM： To investigate the ameliorative effect of ischemic postconditioning （Ⅰ -postC） on pia mater microcirculation in rats subjected to cerebral ischemia reperfusion （I/R） and its mechanisms. METHODS： Thirty -two male Wistar rats were randomly divided into sham, I/R, Ⅰ -postC, and ischemic preconditioning （IPC） groups. The global cerebral I/R injury was induced by shunting carotid artery in rats. Pia mater microcirculation and cerebral microcirculatory perfusion were measured after reperfusion. The content of soluble intercellular adhesion molecule - 1 （ sICAM - 1 ） in plasma was detected using enzyme linked - immunosorbent assay （ ELISA ）. Myeloperoxidase （ MPO ）, malondialdehyde （MDA）, and superoxide dismutase （SOD） in cerebral tissue were detected. The expressions of vascular endothelial cell cadherin （VE- cadherin） and NF- kB p65 in cerebral tissue were assayed by Western blotting. RESULTS： （1） The disturbance of the blood flow in microvessel induced by I/R was improved significantly by Ⅰ - postC. In addition, Ⅰ - postC alleviated significantly the decrease in diameters of microvesseles, cerebral microcireulatory perfusion and cerebral VE - cadherin content induced by I/R （P〈0. 05）. （2） sICAM - 1 in plasma, MPO and MDA in cerebral tissue decreased, but SOD activity in cerebral tissue increased in Ⅰ - postC group, compared with those in I/R group （ P 〈 0.05 or P 〈 0. 01 ）. The over- expression of NF- kB p65 induced by I/R was relieved by Ⅰ- postC （P 〈0. 05）. CONCLUSION： Ⅰ- postC ameliorates pia mater microcirculation in rats subjected to cerebral I/R through suppressing the activation of polymorphonuclear neutrophils mediated by ICAM - 1.