论文部分内容阅读
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 changes of N-methyl-D-aspartate (NMDA) receptor-nitric oxide (NO) -cGMP pathway after cerebral ischemia-reperfusion in rats. Methods The bilateral cerebral carotid artery occlusion and caudal bled blood were used to establish the model of ischemia reperfusion in rats. The cerebral cortex, hippocampus, striatum, midbrain and hypothalamus were observed at different time points after operation NMDA receptor activity (3H-MK801 binding), nitric oxide synthase (NOS) activity and cGMP content changes. Results 3H-MK801 bound in the hippocampus, and the striatum showed a persistent increase in both sites. The native NOS (cNOS) peaked in the hippocampus, cerebral cortex and striatum at 3 days after ischemia, while the induction of iNOS ) Activity and cGMP content only in the hippocampus continued to rise, both in the magnitude and trend of the increase is also very similar. Conclusion Activation of NMDA receptor-NO-cGMP pathway may play an important role in hippocampal ischemic nerve injury.