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机构地区:[1]中山医科大学附属第一医院神经内科98级博士研究生,510080 [2]上海华东化工学院顺磁共振室
出 处:《卒中与神经疾病》2000年第2期95-97,共3页Stroke and Nervous Diseases
摘 要:目的 :探讨自由基在高血糖加重大鼠局灶性脑缺血损伤中的作用。方法 :建立大鼠左大脑中动脉梗死 (Middle Cerebral Artery Occlusion,MCAO)模型 ,在证实高血糖可加重局灶性脑缺血损伤的基础上 ,检测正常和高血糖脑缺血后不同时间的自由基水平。结果 :(1 ) MCAO后 2小时 ,高血糖组的神经细胞缺血损伤程度分级显著高于正常血糖组 ,MCAO后 2 4小时 ,高血糖组的脑梗死面积显著大于正常血糖组 ;(2 )用电子自旋共振 (ElectronSpin Resonance,ESR) PBN自旋捕捉技术直接测定缺血区脑组织自由基水平 ,发现 MCAO后 6小时 ,高血糖组显著高于正常血糖组 ;(3)高血糖组与正常血糖组比较 :超氧化物歧化酶 (SOD)在缺血后 2、6、2 4小时均显著减低 ,脂质过氧化产物丙二醛 (MDA)在缺血后 6、2 4小时显著增高。结论Objective: To investigate the effects of free radicals on hyperglycemiaexaggerated cerebral ischemic injury. Methods: On the basis of middle cerebral artery occlusion(MCAO) model in rats,free radicals were detected in hyperglycemic rats and normoglycemics. Results:(1) In 2 hours MCAO,the grade of ischemic neuronal damage in hyperglycemic rats was significantly higher than in normoglycemics;The infarct area was significantly larger in hyperglycemic rats than in normoglycemics after 24 hours of MCAO.(2) The signal of PBN spinadducts detected by ESR after 6 hours of MCAO was markedly higher in hyperglycemic animals than that in normoglycemics;Hyperversus normoglycemic rats SOD activity were significantly lower after all course of MCAO and higher MDA concentration after 6、24 hours of MCAO.Conclusion:The results show that hyperglycemiaexaggerated cerebral ischemic injury is related to the elevation of free radical formation.
分 类 号:R743.302[医药卫生—神经病学与精神病学]
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