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赵吉清, 吴强, 董兆君, 王仕丽, 李云鹏, 刘勇, 魏相德. 高原缺氧复合梭曼中毒脑Ca2+/CaMPKⅡ活性抑制机理[J]. 中国公共卫生, 2002, 18(1): 89-90. DOI: 10.11847/zgggws2002-18-01-52
引用本文: 赵吉清, 吴强, 董兆君, 王仕丽, 李云鹏, 刘勇, 魏相德. 高原缺氧复合梭曼中毒脑Ca2+/CaMPKⅡ活性抑制机理[J]. 中国公共卫生, 2002, 18(1): 89-90. DOI: 10.11847/zgggws2002-18-01-52
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ZHAO Ji-qing, . Mechnism of Inhition of Ca2+ /CaM-PKⅡ after Combined Soman and Hypoxia Injury[J]. Chinese Journal of Public Health, 2002, 18(1): 89-90. DOI: 10.11847/zgggws2002-18-01-52
Citation: ZHAO Ji-qing, . Mechnism of Inhition of Ca2+ /CaM-PKⅡ after Combined Soman and Hypoxia Injury[J]. Chinese Journal of Public Health, 2002, 18(1): 89-90. DOI: 10.11847/zgggws2002-18-01-52
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高原缺氧复合梭曼中毒脑Ca2+/CaMPKⅡ活性抑制机理

Mechnism of Inhition of Ca2+ /CaM-PKⅡ after Combined Soman and Hypoxia Injury

    摘要
  • 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4000m高原缺氧复合梭曼中毒后12,24,48h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24h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48h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.

     

    Abstract: ObjectiveTo study the mechanism of inhition of Ca2+/CaM-PKⅡ activity after combined soman and hypoxia injury.MethodsThe changes of the content of CaM and activity of Ca2+/CaM-PKⅡ were studied in brain tissue after combined soman and hypoxia injury with RIA for 12,24,48 hours.ResultsThe changes of the content of CaM were significantly higher at soman intoxicated group athypoxia than at soman intoxicated group and control group athypoxia;but the activity of Ca2+ /CaM-PKⅡ were significantly decreased;calcium antagonist Nimodipine,antagonized inhibition of Ca2+/CaM-PKⅡ activity.ConclusionCaM and Ca2+/CaM-PKⅡ lead to important role in the brain damage after combined soman and hypoxia injury.

     

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