脑缺血后大鼠海马及纹状体一氧化氮合酶阳性神经元的变化

夹闭大鼠双侧颈总动脉２ｈ后，用还原型尼克酰胺腺嘌呤二核苷酸脱氢酶反应观察了大鼠海马及纹状体一氧化氮合酶阳性神经元的变化及神经损伤。结果显示：在缺血损伤严重的ＣＡ１区及齿状回一氧化氮合酶阳性神经元较正常动物明显增多并深染，而在同样严重受损的纹状体一氧化氮合酶阳性神经元较正常者明显减少。结合文献及本结果提示：一氧化氮在脑缺血所致的神经损伤中起着重要作用，而海马、纹状体的一氧化氮合酶阳性神经元本身可能具有不同的抗伤害机制．

ISCHEMIA-INDUCED CHANGES OF NITRIC OXIDE SYNTHASE-POSITIVE NEURONS IN THE HIPPOCAMPUS AND THE STRIATUM IN RATS

Changes of nitric oxide synthase (NOS)-positive neurons and neuronal damage of the hippocampus and the striatum were investigated with nicotinamide adenosine dinucleotide phosphate diaphorase (NADPH-d) reaction following bilateral common carotid artery occlusion. The results showed that the neurons in the CA1 area, dentate gyms and the striatum were damaged seriously. NOS-positive neurons increased markedly and were stained densely in the CA1 area and dentate gyrus, while NOS-positive neurons of the striatum decreased obviously. The results indicated that NO played an important role in ischemia induced neuronal damage,and there might exist different mechanisms for NOS-positive neurons resisting injury in the CA1area and the striatum.