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

来源 :中国急救医学 | 被引量 : 0次 | 上传用户:xiawa371236585
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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。 Objective To observe the relationship between cerebral ischemia and inducible nitric oxide synthase (iNOS) gene expression and histopathology and the effects of mild hypothermia. Methods 30 gerbils were divided into three groups: sham - operation group, ischemia group and mild hypothermia group (temporal muscle temperature of 33 ℃, 12h). The bilateral common carotid arteries were occluded for 30 min and reperfusion for 24 and 48 h. And histopathological changes. Results In situ hybridization showed that the expression of iNOS gene in glioma cells was hippocampus. The part of CA1 neurons in the hippocampus was partially shrunk and disappeared. Compared with the ischemia group, the iNOS positive cells in the mild hypothermia group were significantly decreased and the gray scale value was also obvious Decreased (P <0.01), the structure of neurons was normal. Conclusions Mild hypothermia inhibits the expression of iNOS gene and the degree of tissue damage in hippocampus after cerebral ischemia, which may be one of the mechanisms of cerebral protection.
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