大鼠脑缺血再灌后NMDA受体、NO及cGMP含量的变化

Role of N methyl D aspartat Receptor Nitric Oxide cyclic Guanosin Monophosphate Pathway in Ischemic Brain Injury

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。方法采用大鼠双侧颈总动脉阻断和尾部放血并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ＮＯＳ（ｃＮＯＳ）于缺血后３天在海马、大脑皮层、纹状体达高峰；而诱导型（ｉＮ－ＯＳ）活性及ｃＧＭＰ含量仅在海马呈持续上升，两者在增加幅度与趋势上也很相似。结论在海马缺血性神经损伤过程中，ＮＭＤＡ受体－ＮＯ－ｃＧＭＰ通路激活可能起重要作用。

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.