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急性局灶性脑缺血性脑损伤发生机制
引用本文:王兴勇,黄斌,匡凤梧,卢仲毅,许峰.急性局灶性脑缺血性脑损伤发生机制[J].西部医学,2004,16(3):203-205.
作者姓名:王兴勇  黄斌  匡凤梧  卢仲毅  许峰
作者单位:重庆医科大学儿童医院,重庆,400014
基金项目:重庆市科发科研基金资助项目 (NO:2 0 0 1 - 54- 84)
摘    要:目的 探讨急性局灶性脑缺血时脑损伤的发生机制。方法 采用线栓法建立大鼠局灶性脑缺血动物模型 ,结合脑组织含水量及病理变化 ,测定脑缺血 2小时后脑组织 MDA、SOD、GSH- Px、CAT及 NOS活性。结果 缺血性脑损伤时脑组织 MDA、SOD及 NOS活性较对照组升高 ,而 GSH- Px、CAT活性明显下降 ,伴随脑含水量增加 ,出现明显病理改变。结论 氧自由基参与急性局灶性缺血脑损伤的病理过程。

关 键 词:脑损伤  缺血  自由基
文章编号:1672-3511(2004)03-0203-03
修稿时间:2004年1月1日

Pathogenesis of acute focal ischemic cerebral injury
WANG Xing yong,HUANG Bin,KUANG Feng wu,et al..Pathogenesis of acute focal ischemic cerebral injury[J].Medical Journal of West China,2004,16(3):203-205.
Authors:WANG Xing yong  HUANG Bin  KUANG Feng wu  
Abstract:Objective To study the pathogenesis of acute focal ischemia cerebral injury.Methods Establishing the animal model of focal cerebral ischemia by using suture method in mature Wistar rats, detecting the brain water content and pathological changes as well as the activity of malonaldehyde (MDA), superoxides dismutase (SOD), nitric oxide synthase (NOS), glutathione peroxidase (GSH Px), catalase (CAT) in brain tissue after two hours of cerebral ischemia.Results The activity of MDA,SOD, and NOS was higher, but GSH, Px, and CAT was lower in ischemic brain tissues than control ones, concomitanting the increase of brain water content and evident pathological changes.Conclusion Oxygen free radicals have been found to participate in the pathological process of acute focal ischemic cerebral injury.
Keywords:Cerebral injury  Ischemia  Free radicals
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