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脑缺血后脑组织诱生型一氧化氮合酶组织病理学及轻度低温对其影响

Effect of mild hypothermia on inducible nitric oxide synthase and pathological change following ischemia and reperfusion injury

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【作者】 刘雪平冷珍璞劳萍王凤焰薛瑞贤

【Author】 LIU Xue-ping, LENC Zhen -pu, LAO Ping, et al . (Shandong Provincial Hospital,Jinan 250021, China)

【机构】 山东省立医院!济南250021

【摘要】 目的观察脑缺血与诱生型一氧化氮合酶(iNOS)基因表达和组织病理的关系及轻度低温的影响。方法沙鼠30只分假手术组、缺血组及轻度低温组(颞肌温度 33℃,12h),夹闭双侧颈总动脉30 min,再灌注24、48 h检测脑组织iNOS基因表达及组织病理变化。结果原位杂交显示缺血组胶质细胞等呈现iNOS基因表达,海马区CA1神经细胞部分皱缩及缺失,轻度低温组与缺血组相比iNOS阳性细胞明显减小,灰阶值也有明显下降(P<0.01),神经元结构基本正常。结论轻度低温抑制脑缺血后脑组织iNOS 基因表达及减轻海马区组织损害程度可能是其脑保护机制之一。

【Abstract】 Objective To observe the effect of mild hypothermia on inducible nitric oxide synthase (iNOS)and pathological change following cerebral ischemia and reperfusion injury. Methods 30 gerbils were divided into 3 groups:Sham - operated,ischemia, mild hypothermia (temporal muscles remain 33℃, 12h). Cerebral ischemia last 30 win by occluding bilateral common carotid and arterial and reperfuction for 24 h,48 h. INOS gene expression was detected by the situ hybrization and pathological change was observed by HE. Results INOS gene expression in ischemia group was presented in glial cell etc.Compared with is- chemia grovp, mild hypothermia induced down regulation of iNOS gene expression and decreased the pathological change of postischemic pyramidal neurons.Con- clusion Mild hypothermia which inhibited the iNOS gene expression and reduced the extent of pathological change may be one of the protective mechanisms on cerebral ischemia..

  • 【文献出处】 中国急救医学 ,CHINESE JOURNAL OF CRITICAL CARE MEDICINE , 编辑部邮箱 ,2000年04期
  • 【分类号】R363
  • 【被引频次】8
  • 【下载频次】42
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