摘要
目的：观测Ｎ－甲基－Ｄ－天冬氨酸（ＮＭＤＡ）受体在脑损伤后的变化规律以及与继发性脑水肿发生和发展的关系。方法：用放射性配基结合分析法对伤后不同时间的大鼠伤侧大脑皮质ＮＭＤＡ受体活性进行测定；用干湿法测伤后伤侧皮质水含量。结果：ＮＭＤＡ受体活性（Ｂｍａｘ）于伤后３０ｍｉｎ迅速上升达高峰，脑水肿于伤后６～２４ｈ最明显；用ＮＭＤＡ受体的竞争性拮抗剂ＡＰ５（２－ａｍｉｎｏ－５－ｐｈｏｓｐｈｏｎｌａｎｏｉｃａｃｉｄ）治疗后，脑水肿及ＮＭＤＡ受体活性与损伤组比较明显降低。结论：脑损伤后释放的谷氨酸可通过激活ＮＭＤＡ受体而发挥神经元兴奋毒作用。
AIM To study the changes of NMDA (N-methyl-D-aspartate) receptor activities and its relationship to secondary brain edema after brain injury. METHODS:NMDA receptor activities of neuronal membrane in the brain cortex were detected by using a radio ligand binding assay at different time after brain injury, the water contents of brain cortex were measured by dry-wet method.RESULTS: B max of NMDA receptor increased significantly and reached the peak at 30 minutes and the increase of water contents were obvious from 6 to 24 hours after brain injury; After treated with AP 5(2-amino-5-phosphonlanoic acids), a selective NMDA receptor antagonist, the water contents and NMDA receptor antagonist, the water contents and NMDA receptor activities on neuron membrane decreased significanty compared to normal control group.CONCLUSION:Released glutamic acid might generate excitatoxic effect by activating NMDA receptor after brain injury.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1999年第5期450-452,共3页
Chinese Journal of Pathophysiology
