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作 者:王君宇[1] 项乃强[1] 叶鲜明[1] 吴浩强[1] 潘伟生[1]
出 处:《湖南医科大学学报》1999年第2期189-191,共3页Bulletin of Hunan Medical University
摘 要:利用Marmarou氏脑损伤动物模型,测定大鼠脑损伤后不同时间和部位的丙二醛(MDA)含量。结果示:损伤后1h,额叶、顶叶、脑干等处的MDA水平分别比对照组高出367%,418%和351%(P<0.01),并持续增高,伤后4h达高峰后缓慢下降,伤后24h仍明显高于对照组。纹状体、颞叶等处伤后1h的MDA水平升高较上述部位稍低,而分别较对照组升高169%和133%(P<0.01),伤后4h虽仍持续升高,但不超过35%。提示在大鼠弥漫性脑损伤后短期内即有自由基生成,几乎波及脑内各个部位,但程度不一。Objective: Using a diffuse brain injury animal model, we studied the time course of lipid peroxidation in different regions of injured rat brains. Methods: 53 male SD rats were randomly divided into sham, post traumatic 1,2,4,7,24h groups ( n =8) to measure the MDA(malondialdehyde) at the bilateral frontal, temporal, parietal, striatum and brain stem, another 5 rats were researched for histological study. Results: At the frontal, parietal and brain stem, the MDA levels were 36.7%, 41.8% and 35.1%, respectively, higher than sham at one hour after injury ( P <0.01). The MDA levels in these regions continued to increase and peaked at 4 hours after the injury. The levels decreased slowly, and by 24 hours, they were still significantly higher than the sham control's. The elevation of MDA levels was less in the striatum and the temporal compared with above regions at one hour. Their rising rates were 16.9% and 13.3%, respectively( P <0.01). The MDA levels in there two regions continued to increase even after 4 hours of injury, but the degree of elevation never exceeded 35%. Conclusion: There is an immediate, post traumatic burst of MDA production, suggesting the formation of free radicals after diffuse head injury. Even though all the regions sampled show the same effect, certain regions are less affected in this diffuse brain injury animal model.
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