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缺血后处理改善脑缺血再灌注大鼠软脑膜微循环
引用本文:姚树桐,刘秀华,汤旭明,孙胜,王家富.缺血后处理改善脑缺血再灌注大鼠软脑膜微循环[J].中国病理生理杂志,2009,25(3):451-455.
作者姓名:姚树桐  刘秀华  汤旭明  孙胜  王家富
作者单位: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
基金项目:国家自然科学基金,国家自然科学基金重大国际合作研究项目 
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-κB p65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-κB p65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。

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  
收稿时间:2008-3-18
修稿时间:2008-9-10

Ischemic postconditioning ameliorates pia mater microcirculation in rats subjected to cerebral ischemia reperfusion
YAO Shu-tong,LIU Xiu-hua,TANG Xu-ming,SUN Sheng,WANG Jia-fu.Ischemic postconditioning ameliorates pia mater microcirculation in rats subjected to cerebral ischemia reperfusion[J].Chinese Journal of Pathophysiology,2009,25(3):451-455.
Authors:YAO Shu-tong  LIU Xiu-hua  TANG Xu-ming  SUN Sheng  WANG Jia-fu
Institution:1Department of Pathophysiology, Chinese PLA General Hospital, Beijing 100853, China; 2Department of Pathophysiology, Taishan Medical College, Taian 271000, China.E-mail:xiuhualiu98@yahoo.com.cn
Abstract: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-κB 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 microcirculatory 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-κB 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.
Keywords:Ischemic postconditioning  Reperfusion injury  Pia mater microcirculation  Intercellular adhesion molecule-1
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