摘要
利用Wistar大鼠制成急性外伤性脑水肿模型,在此基础上检测动物在脑损伤后2、4、8小时脑组织的氧自由基反应产物—脂质过氧化物(LPO),三磷酸腺苷酶(ATPase)活性和脑含水量的变化。研究表明,脑损伤后2小时脑Na^+—K^+—ATPase有明显增高(P<0.05),4、8小时ATPase活性均显著性下降(P<0.01);脑损伤后脑LPO含量和脑含水量显著性增高(P<0.01),随时间延长,增高更明显。我们认为,脑损伤后由于氧自由基的大量产生使ATPase受到明显影响,造成神经组织细胞的不可逆性损害,应用氧自由基清除剂是治疗外伤性脑水肿的关键措施。
We, using Wistar rat model of acute injured cerebral edema, studied the changes of water content, lipidperoxide (LPD) and adenosine triphosphatase (ATPase) activity at hour 2, 4 and 8 following head injury. The resudts showed that at 2 hour after injury, Na^+—K^+—ATPase actvity was significantly increased, the ATPase (Ca^(2+)—Mg^(2+)—ATPase. Na^+ —Ka^+—ATPase) activity was markedly reduced at hour 4 and 8, the water content and LPO were significantly increased after injury. We considered oxygen free radical could cause marked inhibition of membranal enzyme activity, and play an important role in traumatic hrain edema. Using oxygen free radical scavengers might be agood method in the treatment of brain injury and relavent brain edema.
出处
《中华创伤杂志》
CAS
CSCD
北大核心
1993年第3期145-147,共3页
Chinese Journal of Trauma
关键词
颅脑损伤
脑水肿
氧
自由基
Brain injury Brain edema Oxygen free radical Na^+-K^+-ATPase Ca^(2+)-Mg^(2+)-ATPase
