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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 model of global cerebral ischemia-reperfusion was established by rat 4-vessel occlusion (4VO). The changes of Na + K + -ATPase activity in hippocampus, neocortex and subcortex were observed at different phases of ischemia and reperfusion. The hippocampal Na + K + -ATPase activity decreased immediately after ischemia (P <0.05), and there was a transient decrease in the activity of neocortex and cortex after reperfusion. The hippocampus enzyme activity did not recover after 168h of reperfusion (P < 0.05). The decrease of Na + K + -ATPase activity is related to the direct destruction of the enzyme structure by free radicals, the degradation of membrane phospholipids and the change of interfacial lipid or membrane fluidity due to the unsaturated fatty acid peroxide.