大鼠脑缺血再灌注NMDA受体,NO及cGMP含量的变化

目的 观察大鼠脑缺血再灌后Ｎ－甲基－Ｄ－天冬氨酸（ＮＭＤＡ）受体－一氧化氮（ＮＯ）－ｃＧＭＰ通路变化。方法 采用大鼠以侧颈总动脉阻断和尾部放血产重复缺血再灌的脑缺血模型,观察术后不同时间动物大脑皮层、海马、纹状体、中脑和下丘脑５个部位的ＮＭＤＡ受体活性（＾３Ｈ－ＭＫ８０１结合）、一氧化氮合酶（ＮＯＳ）活性及ｃＧＭＰ含量变化。结果 ＾３Ｈ－ＭＫ８０１结合在海马、纹状体两部位呈持续性明显增加;原生型Ｎ

Role of N-methyl-D-aspartat receptor-nitric oxide-cyclic guanosin monophosphate pathway in ischemic brain injury

OBJECTIVE: To observe the role of NMDA receptor-Nitric Oxide(NOS)-cGMP pathway in ischemic brain injury. METHODS: The common cervical arteries of the rats were transient blocked bilaterally, in association with bleeding from their tails and followed by reperfusion. The procedures were repeated once again as above to establish a stable ischemic brain injury model. 3H-MK801 binding, cNOS activity, iNOS activity, and the cGMP content were measured at different time intervals after ischemic injury. RESULTS: The results indicated that the change of 3H-MK801 binding varied among the cerebral cortex and hippocampus. cNOS activity began to rise in all parts of the brain 24 hours after operation and reached its peak in 3 days. The regions where iNOS and cNOS activity and cGMP content all increased significantly include the hippocamus, striatum and cortex, especially in hippocampus. CONCLUSIONS: The tendency and degree of increase of those four indixes were cosistent during ischemic injury, indicating an important role of NMDA receptor-NO-cGMP in ischemic injury of the hippocampus.