摘要
目的:探讨脑出血后血肿周围脑组织自由基氧化损害的机制。方法:SD大鼠随机分为脑出血组和假手术组。采用立体定向自体血注入大鼠尾状核建立ICH模型,观察各组术前及术后各时点血肿周围脑组织超氧化物歧化酶(SOD)活力和丙二醛(MDA)含量,含水量及神经功能障碍评分变化。结果:脑出血组术后各时点SOD活力明显低于假手术组,而术后各时点MDA含量显著高于假手术组。脑出血组术后各时点含水量与SOD活力呈负相关,与MDA含量呈正相关。脑出血组术后各时点神经功能障碍评分与SOD活力呈正相关,与MDA含量呈负相关。结论:脑出血大鼠血肿周边脑组织有明显的氧化损伤,此损伤可能是脑出血后脑水肿形成和脑损伤机制之一。
Objective： To explore the mechanism of oxidation damage of free radicals after intracerebral hemorrhage （ICH）. Methods： SD rats were assigned randomly to two groups： namely, the sham operation group and the ICH group. Intracerebral hemorrhage was induced in rats by injecting autologous blood into the left caudate. The activity of superoxide dismutase（SOD） and the content of malondialdehyde（MDA） in perihematoma were detected. Water contents in perihematoma at various stages were examined and neurobehavioral outcome at various stages was assessed. Results： The activity of SOD post operation in ICH group was found lower than that in sham operation group and the content of MDA post operation in ICH group was found higher than that in sham operation group. Water contents post operation in ICH group were significantly negatively correlated witfi the activity of SOD while they were significantly positively correlated with the content of MDA. Neurobehavioral scores post operation in ICH group were significantly positively correlated with the activity of SOD while they were significantly negatively correlated with the contents of MDA. Conclusion： The rats with ICH showed significant oxidation damage in perihematoma, which may be the underlying pathophysiologic mechanism of brain edema and brain damage following ICH.
出处
《泸州医学院学报》
2005年第5期417-419,共3页
Journal of Luzhou Medical College
关键词
脑出血
超氧化物歧化酶
丙二醛
脑水肿
脑损伤
Intracerebral hemorrhage
Superoxide dismutase
Malondialdehyde
Brain edema
Brain damage
