缺血后处理改善脑缺血再灌注大鼠软脑膜微循环  

Ischemic postconditioning ameliorates pia mater microcirculation in rats subjected to cerebral ischemia reperfusion

作　　者：姚树桐[1,2] 刘秀华[1] 汤旭明[1] 孙胜[1] 王家富[2] 

机构地区：[1]中国人民解放军总医院病理生理研究室,北京100853 [2]泰山医学院病理生理学教研室,山东泰安271000

出　　处：《中国病理生理杂志》2009年第3期451-455,共5页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目(No.30670822);国家自然科学基金重大国际合作资助项目(No.30620130111)

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-κBp65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-κBp65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。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.

关 键 词：缺血后处理 再灌注损伤 软脑膜微循环 胞间黏附分子-1 

分 类 号：R331.3[医药卫生—人体生理学]