摘要
用双侧颈总动脉夹闭加放血方法造成大鼠一过性不完全性脑缺血及再灌注模型 ,以还原型尼克酰胺腺嘌呤二核苷酸脱氢酶 ( NADPH-d)组织化学方法对缺血再灌注期间海马 CA1 区内一氧化氮合酶阳性神经细胞变化进行研究。结果发现 ,海马 CA1 区神经细胞受损 ,在缺血 3 0 min时一氧化氮阳性细胞数最高 ( 44 .5± 7.42 ) ,为空白对照组 2倍 ,再灌注 2 h、12 h、2 4h、3 d后逐渐下降 ,5 d时恢复正常水平 ( 2 1.12± 3 .5 0 )。研究表明 ,不完全性脑梗塞时一氧化氮合酶表达与海马 CA1
The rat models of incomplete cerebral ischemia were acquired by bilateral carotid artery clamping combined with bleeding. NADPH-diaphorase histochemistry was used to investigate the postischemia changes of nitric oxide synthase (NOS) in the hippocampal CA 1 area in the model. The results showed that the neurons in the hippocumpos CA 1 area were damaged. The number of NOS-positive cell in CA 1 was maximal to about 2 times higher than the normal control group in hippocampal CA 1 at 30 min following incomplete ischemia and was decreased gradually at 2h, 12h, 24h, 3d after reperfusion and was normal level in 5d. The result suggest that NO may play a role in delayed neuronal death and there may be some correlation between the NOS expression and vulnerability of neurons in hippocampal CA 1 area.
出处
《南通医学院学报》
1999年第4期403-405,共3页
ACTA Academiae Medicinae Nantong
关键词
脑缺血
海马CA1
一氧化氮合酶
incomplete cerebral ischemia hippocampus CA 1 nitric oxide synthase NADPH-diaphorase rat
