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王仕丽, 赵吉清, 吴强, 李云鹏, 董兆君, 魏相德. 模拟高原梭曼中毒脑组织磷脂酶A2等活性和含量的变化[J]. 中国公共卫生, 2002, 18(1): 87-89. DOI: 10.11847/zgggws2002-18-01-51
引用本文: 王仕丽, 赵吉清, 吴强, 李云鹏, 董兆君, 魏相德. 模拟高原梭曼中毒脑组织磷脂酶A2等活性和含量的变化[J]. 中国公共卫生, 2002, 18(1): 87-89. DOI: 10.11847/zgggws2002-18-01-51
WANG Shi-li, . Changes of PLA2, ATP, ADP, AMP and cAMP on Brain Tissues after Combined Soman and Hypoxia Injury[J]. Chinese Journal of Public Health, 2002, 18(1): 87-89. DOI: 10.11847/zgggws2002-18-01-51
Citation: WANG Shi-li, . Changes of PLA2, ATP, ADP, AMP and cAMP on Brain Tissues after Combined Soman and Hypoxia Injury[J]. Chinese Journal of Public Health, 2002, 18(1): 87-89. DOI: 10.11847/zgggws2002-18-01-51

模拟高原梭曼中毒脑组织磷脂酶A2等活性和含量的变化

Changes of PLA2, ATP, ADP, AMP and cAMP on Brain Tissues after Combined Soman and Hypoxia Injury

  • 摘要: 目的探讨高原缺氧复合梭曼中毒脑组织中磷脂酶A2(PLA2)、腺苷酸、环磷酸腺苷的变化及其在脑损伤中的作用机制.方法以Wistar大鼠为模型观察高原缺氧复合梭曼中毒后12,24,48h大鼠脑水肿的发生率以及脑组织中PLA2的活性、腺苷酸、环磷酸腺苷(cAMP)的变化特点.结果高原缺氧复合梭曼中毒后24h脑组织伊文思蓝含量(EB)、PLA2的活性、腺苷酸含量明显升高以及海马、小脑、皮层cAMP的含量明显升高.结论高原缺氧复合梭曼中毒时,脑组织损伤具有早而重的特点.其具体机制可能与能量代谢抑制及衰竭和磷脂酶A2和腺苷酸环化酶的激活有关.

     

    Abstract: ObjectiveTo study the mechanism of the effect of PLA2 on the damage of brain tissues after combined soman and hypoxia injury.MethodsThe changes in cAMP,ATP,ADP,AMP,PLA2,Evans blue,water contents of brain tissue were studied in the Wister after the combined soman and acute hypoxia injury with microtitration,albumin labelled with Evans blue,RIA,and electron micropy for 12,24,48 hours.ResultsThe changes of the content of cAMP,ATP,ADP,AMP, PLA2,Evans blue were sig nificantly higher at soman intoxicated group athy poxia than at soman in toxicated group and control group athypoxia.ConclusionThe damage became more severe at combined soman and hypoxia injury,compared with soman or hypoxia injury,also the damage appeared earlier and more severe.It shows alteration of brain energy metabolism,activation of PLA2,activation of cAMP and their correlation with neuronal damage.

     

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