高压氧对外伤性脑水肿家兔线粒体ATP酶活性的影响

Effect of hyperbaric oxygenation on cerebral mitochondria and ATPase activity in traumatic cerebral edema of rabbits

目的 研究外伤性脑水肿后脑细胞线粒体ATP酶活性、丙二醛 (MDA)含量在继发性脑损伤中的作用 ,以及高压氧治疗的机理。方法 应用家兔脑损伤模型 ,观察高压氧作用后不同时间脑含水量、线粒体ATP酶活性、MDA含量变化。结果 线粒体ATP酶活性在伤后 4h即开始下降 ,至 48h降到最低点 ,MDA含量伤后显著增加 ,随时间延长增加更加明显 ,MDA与脑含水量间呈正相关 ,ATP酶活性与脑含水量之间呈负相关 ,高压氧组与外伤组比较 ,上述指标变化均较轻。结论 脑外伤后脑细胞线粒体自由基反应增强 ,ATP酶活性受抑 ,促进脑水肿发生、发展 ,高压氧通过减少自由基。

Objective To study the alterations of cerebral mitochondria,malonyl-dialdehyde(MDA) and ATPase activity after traumatic cerebral edema,and explore the effects and mechanism of hyperbaric oxygenation(HBO) for the traumatic cerebral edema.Methods Models of rabbit traumatic cerebral edema were first performed.Then,the alterations of cerebral mitochondria,MDA,water-bearing amount and ATPase activity were observed at various periods after HBO treatment.Results The mitochondria and ATPase activity decreased within 4 h after trauma,and kept on descending until 48 h of post-trauma.The MDA was obviously enhanced along with the increase of time after trauma.Moreover,there was positive correlation between the cerebral MDA and water-bearing amount;contrarily,the relationship of ATPase activity and water-bearing amount was negative correlation.When the effects were compared between the HBO group and control group,the above parameters of HBO group were slighter than those of control group.Conclusion Experiment shows that the free radicals produced by mitochondrias are increased after cerebral injury,so,the ATPase activity was inhibited resulting in further occurrence of cerebral edema.Using the HBO treatment,it can reduce the free radicals and enhance the ATPase activity,thus the cerebral edema receives improvement.