Oxygen radicals in brain injury.
Oxygen radicals in brain injury.
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DOI：
10.1089/cns.1986.3.257
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发表时间：
1986
期刊：
影响因子：
--
通讯作者：
H. Kontos;J. Povlishock
中科院分区：
文献类型：
--
作者：
H. Kontos;J. Povlishock
在麻醉猫中的实验性液压冲击脑损伤引起血管损伤，其特征在于持续的小动脉扩张、对血管收缩剂和血管扩张剂干预的异常反应、局灶性内皮损伤和血管壁的耗氧量减少。通过用环氧合酶抑制剂或氧自由基清除剂预处理，这些异常被最小化或完全抑制。因此，它们被归因于通过环氧合酶加速花生四烯酸代谢过程中产生的氧自由基。在这种类型的脑损伤后，脑中磷脂酶c的活性增加，并且脑中的野牡丹素浓度短暂增加。超氧阴离子自由基检测在脑损伤后立即以及一小时后的超氧化物歧化酶的硝基四氮唑还原的可降解部分的脑细胞外空间。超氧化物歧化酶和过氧化氢酶也可逆转脑损伤后脑小动脉的持续扩张和异常反应。这些结果表明，用氧自由基清除剂治疗可能有效地抑制或逆转脑损伤的一些影响，即使用治疗剂的干预发生在损伤发生后的某个时候。
Experimental fluid percussion brain injury in anesthetized cats causes vascular injury characterized by sustained arteriolar dilation, abnormal reactivity to vasoconstrictor and vasodilator interventions, focal endothelial lesions, and reduction of the oxygen consumption of the vessel wall. These abnormalities are minimized or completely inhibited by pretreatment with cyclooxygenase inhibitors or with oxygen radical scavengers. They were therefore ascribed to oxygen radicals generated in the course of accelerated arachidonate metabolism via cyclooxygenase. Following this type of brain injury, there is an increase in the activity of phospholipase c in the brain and a transient increase in brain concentration of prostaglandins. Superoxide anion radical was detected in the extracellular space of the brain both immediately following brain injury as well as one hour afterwards as the superoxide dismutase inhibitable portion of nitroblue tetrazolium reduction. The sustained dilation and abnormal reactivity of cerebral arterioles following brain injury were also reversed by superoxide dismutase and catalase applied on the brain surface 30 minutes after injury. These results suggest that treatment with oxygen radical scavengers might be effective in inhibiting or reversing some of the effects of brain injury, even though the intervention with the therapeutic agents occurs sometime after the injury has taken place.