氯胺酮对脑缺血诱导大鼠海马、皮层一氧化氮变化的影响

EFFECT OF KETAMINE ON THE CHANGE OF NO IN HIPPOCAMPUS AND CEREBRAL CORTEX AFTER ACUTE CEREBRAL ISCHEMIA

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 ,5 0mg/kg的给药量差异显著 (P <0 0 5 )。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 。

Objectives:To explore the pathological mechanisms of Nitric oxide (NO) after acute cerebral ischemia.Methods:By nitrate reductase method,the abnormal changes of the content of NO in hippocampus were studied and also the cerebral cortex after rat forebrain ischemia and the effect of ionic channel antagonist ketamine on them.Results:①NO concentrations in hippocampus and cerebral cortex increased,which was high first,then decreased gradually.②Injection of ketamine before ischemia,the release of NO was lower conspicuously than that of the control group.There were significant differences in the administration group of 50mg/kg (P<0 05).Conclusions:Ionic channel antagonist ketamine can inhibit partly the abnormal release of NO in cerebral ischemia,and the change of NO induced by early cerebral ischemia might be the stress of brain on environmental stimulation.