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作 者:陈光辉[1] 胡亚贤 母敬郁 杨俊英[1] 常明[1] 饶明俐[1]
机构地区:[1]白求恩医大一院,南京军区南京总医院,白求恩医大基础生化教研室
出 处:《中风与神经疾病杂志》1996年第4期204-206,共3页Journal of Apoplexy and Nervous Diseases
摘 要:应用大鼠4血管关闭(4VO)方法制作全脑缺血再灌流模型,观察海马、新皮层及皮层下结构在缺血及再灌流不同时相Na+K+─ATP酶活性变化。缺血时即刻出现海马Na+K+─ATP酶活性降低(P<0.05),再灌流后新皮层及皮层下酶活性有暂时性降低,海马的酶活性在再灌流168h时仍未恢复(P<0.05)。Na+K+─ATP酶活性的降低与自由基对酶结构的直接破坏、膜磷脂降解以及不饱和脂肪酸过氧化引起界面脂或膜流动性改变有关。The Na+K+-ATPase activites in hippocampus, subcortex(including thalamus and striatum) and neocortex of Wistar rat brain during ischemia and different reperfusion periods were determined. The results showed that ischemia had the different effects on Na+, K+-ATPase activity of the three regions. Only in hippocampus was the Na+ ,K+-ATPase activity lower than that of sham-operated group until reperfusion 168h, The decrease of Na+. K+-ATPase activity might result from (1) free radical initiating the oxidation of SH groups, causing conformational changes, (2)the degradation of phospholipids altering the microenvironment of the enzyme protein,(3) the ratio of PC to SM influencing membrane fluidity.
关 键 词:脑缺血 海马 ATP酶 再灌注损伤 钠离子 钾离子
分 类 号:R743.31[医药卫生—神经病学与精神病学]
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