摘要
用四血管闭塞法造成大鼠一过性全脑缺血。按不同时程，以还原型尼克酰胺腺嘌呤二核苷酸脱氨酶组织化学方法对再灌流期间海马不同亚区内一氧化氮合酶阳性细胞的数量变化进行了研究。结果发现：海马本部的一氧化氮合酶阳性细胞数量在再灌流2～6h即有增高，到12～24h进一步增加至对照水平的3倍左右；3d时已有所减少，7d时在CA1区恢复至对照组的水平。齿状回的一氧化氮合酶阳性细胞数量在再灌流2～6h已有明显的增高，约为对照水平的2倍．并在再灌流12h、24h和3d时保持在同一水平。此外，缺血后各亚区内染出的血管数量于再灌流2～6h即有明显增多，并在再灌流7d后仍明显高于对照组。本文结合文献对缺血性神经元坏死和一氧化氮合酶表达之间的关系进行了讨论。
Pyramidal cells in different hippocampal subfield show different vulnerability to transient cerebral ischemia. In this study, we used NADPH-diaphorase histochemistry to investigate the postischernic changes of nitric oxide synthase (NOS) in different hipPOcampal sub fields in a rat model of cerebral ischemia. Rats subjected to 15 min of 4-vessel occlusion were fixed by perfusion fixation 2～6, 12, 24 h, and 3, 7 d after recirculation and the density 0f NOS p0sitive cells in CA1, CA2-3, and dentate gyrus was counzed respectively,. A transient increase in the number of NADPH-diaphorase positive cells, beginning 2～6 h and maximal to about 3 times higher than the control level 12～24 h following ischemia, was 0bserved in CA1 and CA2-3 sub fields.In dentate gyrus, the number was doubled 2～6 h after ischemia and kept at almost the same Ievel in 12 h, 24 h, and 3 days following ischemia. In addition, 2～6 h after ischemia, the number of NADPH-diaphorase positive microvasa increased, and it was still remarkably higher than the control Ievel even after 7 days of recirculation. The result suggests that NO may play a r0Ie in the course of delayed neuronal death, and there may be some corelations between the NOS expressi0n and ischemic vulnerability in hippocampal subfields.
出处
《神经解剖学杂志》
CAS
CSCD
北大核心
1998年第1期8-12,共5页
Chinese Journal of Neuroanatomy
关键词
脑缺血
一氧化氮合酶
海马
transient cerebral ischemia, nitric oxide synthase,NADPH-diaphorase, hippocampus, rat
