EFFECT OF KETAMINE ON THE CHANGE OF NO IN HIPPOCAMPUS AND CEREBRAL CORTEX AFTER ACUTE CEREBRAL ISCHEMIA
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摘要: 目的:探讨一氧化氮在急性全脑缺氧缺血的病理作用机制.方法:用硝酸还原酶特异性还原一氧化氮(NO)产物的方法,测定大鼠前脑缺血模型中海马、皮层一氧化氮释放量的异常变化及离子通道拮抗剂氯胺酮对这些变化的影响.结果:①急性脑缺血后海马、皮层胞内一氧化氮含量有不同程度的增高,呈先升后降的趋势.②预先腹腔注射氯胺酮,大鼠海马、皮层NO释放量明显低于对照组,50mg/kg的给药量差异显著(P＜0.05).结论:一定量的离子通道拮抗剂氯胺酮能部分抑制缺血性中枢神经元一氧化氮的异常释放,且早期脑缺血诱生一氧化氮的异常升高很可能是脑组织对外界刺激的应激反应.
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