高原缺氧复合梭曼中毒脑Ca^(2+)/CaMPKⅡ活性抑制机理  

Mechnism of Inhition of Ca^(2+) /CaM-PKⅡ after Combined Soman and Hypoxia Injury

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]第三军医大学毒理学教研室,重庆400038

出　　处：《中国公共卫生》2002年第1期89-90,共2页Chinese Journal of Public Health

摘　　要：目的　探讨缺氧复合梭曼中毒脑组织Ca2 + /CaMPKⅡ活性抑制机理。方法　本实验采用放射免疫技术 ,观察模拟 4 0 0 0m高原缺氧复合梭曼中毒后 12 ,2 4 ,4 8h脑组织CaM含量以及钙 /钙调蛋白激酶Ⅱ (Ca2 + /CaM -PKⅡ )活性的变化影响。结果　高原缺氧复合梭曼中毒后脑组织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 4 8h明显低于单纯中毒组、缺氧对照组和正常对照组 ;而钙通道拮抗剂尼莫地平 (Nimodipine)可对抗这种改变。结论　CaM、Ca2 + /CaM -PKⅡ在高原缺氧复合梭曼中毒大鼠脑组织损伤机理中起了重要的作用。Objective To study the mechanism of inhition of Ca 2+ /CaM-PKⅡ activity after combined soman and hypoxia injury.Methods The changes of the content of CaM and activity of Ca 2+ /CaM-PKⅡ were studied in brain tissue after combined soman and hypoxia injury with RIA for 12,24,48 hours.Results The changes of the content of CaM were significantly higher at soman intoxicated group at hypoxia than at soman intoxicated group and control group at hypoxia;but the activity of Ca 2+ /CaM-PKⅡ were significantly decreased;calcium antagonist Nimodipine,antagonized inhibition of Ca 2+ /CaM-PKⅡ activity.Conclusion CaM and Ca 2+ /CaM-PKⅡ lead to important role in the brain damage after combined soman and hypoxia injury.

关 键 词：缺氧 梭曼中毒 脑组织 Ca^2+/CaMPKⅡ 

分 类 号：R827.12[医药卫生—临床医学]