磷脂酶A2在模拟高原梭曼中毒性脑损伤中的变化

目的 探讨磷脂酶A2（PLA2）在缺氧复合梭曼中毒脑损伤的作用机制。方法 应用微量滴定，放免法从动物整体水平观察了高原缺氧，梭曼中毒单一与复合致伤后12、24、48h大鼠脑组织含水率（WCB）、伊文思蓝（EB）含量，PLA2的活性，环磷酸腺苷（cAMP)含量的变化。结果 高原中毒组脑组织伊文思蓝含量，PLA2的活性，ADP、AMP、cAMP含量在中毒后24、48h明显高于平原中毒组，高原对照组和正常对照组，应用钙通道阻断剂尼莫地平可明显降低PLA2活性，减轻缺氧中毒后脑组织水肿。结论 磷脂酶A2、腺苷酸环化酶的激活可能参与高原缺氧复合梭曼中毒脑损伤。

Changes of PLA2 in the brain of soman intoxication combined with hypoxia

Objective To clarify the mechnisim of PLA 2 in the brain of soman intoxication combined with hypoxia injury. Methods cAMP,PLA 2,Evans blue (EB) and water content of the brain tissue (WCB) were measured in rat after combined soman and acute hypoxia injury with microtitration and RIA. Results The level of cAMP, Evans blue and PLA 2 activity were significantly higher in soman intoxication combined hypoxia than that of simple soman intoxication group, simple hypoxic group at 24, 48 h and Control group. Additionally, nimodipine was effective in inhibiting PLA 2 activity and reducing brain edema. Conclusion Activation of PLA 2 and cAMP are involved in the damage of the brain in combined soman and hypoxia injury.