谷氨酸在模拟高原梭曼中毒性脑损伤的作用研究  

Effect of glutamic acid on brain damage in simulated high altitude hypoxia combined soman intoxication

作　　者：赵吉清[1] 吴强[1] 董兆君[1] 王仕丽[1] 李云鹏[1] 刘勇[1] 魏相德[1] 

机构地区：[1]第三军医大学预防医学系毒理学教研室,重庆400038

出　　处：《第三军医大学学报》2001年第6期630-632,共3页Journal of Third Military Medical University

基　　金：全军"九五"指令性课题 (96L0 1 5 )

摘　　要：目的　探讨谷氨酸 (Glutamicacid ,Glu)在缺氧复合梭曼中毒脑损伤的作用机制。方法　采用氨基酸分析和放免技术 ,研究高原缺氧、梭曼中毒单一与复合致伤后 1 2、2 4、4 8h脑组织Glu和CaM含量的变化以及钙 /钙调蛋白激酶Ⅱ (Ca2 +/CaM PKⅡ )活性的影响及其机制。结果　缺氧复合梭曼中毒组脑组织Glu、CaM含量在中毒后 2 4h明显高于单纯中毒组、缺氧对照组和正常对照组 ;缺氧中毒组脑组织Ca2 +/CaM PKⅡ活性在中毒后 2 4h明显低于单纯中毒组、缺氧对照组和正常对照组 ;而N 甲基 D 天冬氨酸(NMDA)受体拮抗剂地佐环平 (MK 80 1 )和钙通道拮抗剂尼莫地平 (Nimodipine)可对抗这种改变。结论　高原缺氧复合梭曼中毒后Glu的兴奋毒引起脑损伤和Ca2 +/CaM PKⅡ的活性下降 ,主要由NMDA受体介导和胞外Ca2 +内流增加有关。Objective To explore the mechanism of glutamic acid (Glu) on brain damage in high altitude hypoxia combined soman intoxication. Methods The content of Glu, CaM and activity of Ca 2+ /CaM PK Ⅱ in brain tissue after hypoxia combined soman intoxication were studed with RIA and amino acid analyzing. Results The content of Glu, CaM were significantly higher in soman intoxicated combined hypoxia group than that in simple soman intoxicated group or simple hypoxia group 24 h after infoxication; but the activity of Ca 2+ /CaM PK Ⅱ were significantly decreased; NMDA receptor antagonist MK801 and calcium antagonist Nimodipine could antagonize EAA induced inhibition of Ca 2+ /CaM PK Ⅱ activity. Conclusion NMDA receptor may be involved in excitotoxicity induced inhibition of Ca 2+ /CaM PK Ⅱ activity in high altitude hypoxia combined soman intoxication.

关 键 词：缺氧 梭曼中毒 谷氨酸 Ca^2+/CaM依赖性蛋白激酶Ⅱ 脑损伤 

分 类 号：R827.172[医药卫生—临床医学] R594.3