外伤性脑水肿脑组织氧自由基与超氧化物歧化酶活性变化的实验研究

Experiment Studies on the Change of Oxygen Free Radicals and Superoxide Dismutase in AcuteTraumatic Brain Edema

本实验在建立Ｗｉｓｔａｒ大鼠急性外伤性脑水肿模型基础上，动态检测脑损伤后脑组织ＬＰＯ、ＳＯＤ和脑含水量，并作病理学光镜观察。结果表明，脑损伤后２ｈ，两大脑半球ＬＰＯ即显著增高；损伤后２ｈ、４ｈ损伤侧大脑半球ＳＯＤ活性显著增高，但ＳＯＤ／ＬＰＯ却明显下降，对侧半球ＳＯＤ变化不大；但８ｈ时两大脑半球ＳＯＤ均显著下降，且ＳＯＤ／ＬＰＯ显著降低，脑含水量与ＩＰＯ的升高呈平行关系，病理观察见外伤性脑水肿以血管源性为主，但同时伴有细胞毒性脑水肿。说明氧自由基是外伤性脑水肿发生、发展的关键性毒在物质，ＳＯＤ尽管早期有代偿性升高，但由于与ＬＰＯ比值下降，仍无法抗衡氧自由基的毒性作用。

e applied the model of acute injured cerebral edema in wistar rats and studied the changes oflipid peroxide (LPO), superoxide dismutase (SOD), water content and morphology in the brain tissue.The experimental results showed that (1) at the second hour following injury, LPO wassignificantly increased in the bilateral hemisphere and it was increased gradually. (2) at the second hour, the 4th hour following injury, SOD activity was found to be significantly increased in the injuriedcerebral hemisphere. At 8th hour following injury, SOD activity was significantly decreased inbilateral hemisphere. But the SOD/LPO ratio was decreased in bilateral hemisphere after injury. (3)Atthe second hour following injury, the water content in the bilateral hemisphere was increased and it was gradually increased. Moreover, the water content in the injured hemisphere wassignificantly higher than that in the no-injured. (4)Under light microscope we found the presence oftypical vasogenic edema and cytotoxic edema. According to the results of our experiments. Weconsider that the brain edema was caused by oxygen free radical. Superoxide dismutase (SOD) wascompensatorily increased in early stage of injury. But it was decreased at the end. SOD/LPO ratio may be used as a critercion to measure the effect of SOD on scavenging the oxygen free radicals.Therefore, we think that oxygen free radical plays an important role in taumatic brain edema. Oxygen free radical scavengers may possibly become a critical therepecutic modality for brain injued and brainedema.