Hall E D
Central Nervous System Diseases Research Unit, Upjohn Company, Kalamazoo, Michigan.
Crit Care Clin. 1989 Oct;5(4):793-805.
This article has reviewed the current knowledge regarding the occurrence and possible role of oxygen radical generation and lipid peroxidation in acute CNS injury. Although much work remains, three criteria required to establish the pathophysiologic importance of oxygen radical reactions in post-traumatic events have been met, at least in part. First, oxygen radical generation and lipid peroxidative reactions appear to be early biochemical events subsequent to CNS injury. Second, a growing body of direct or circumstantial evidence suggests that these reactions are causally linked to pathophysiologic processes such as hypoperfusion, edema, axonal or synaptic conduction failure, and anterograde (Wallerian) degeneration. Third, compounds that inhibit lipid peroxidation or scavenge oxygen radicals can block post-traumatic pathophysiology and promote nervous tissue function and survival in experimental studies. Nevertheless, the importance of oxygen radicals and lipid peroxidation ultimately depends on whether it can be more clearly demonstrated that early application of effective antifree radical or antiperoxidative agents can promote survival and neurologic recovery after CNS injury in humans.
本文回顾了目前关于急性中枢神经系统损伤中氧自由基生成和脂质过氧化的发生情况及可能作用的相关知识。尽管仍有许多工作要做，但确立氧自由基反应在创伤后事件中病理生理重要性所需的三个标准至少部分已得到满足。首先，氧自由基生成和脂质过氧化反应似乎是中枢神经系统损伤后的早期生化事件。其次，越来越多的直接或间接证据表明，这些反应与诸如灌注不足、水肿、轴突或突触传导障碍以及顺行性（沃勒氏）变性等病理生理过程存在因果联系。第三，在实验研究中，抑制脂质过氧化或清除氧自由基的化合物可阻断创伤后病理生理过程，并促进神经组织功能和存活。然而，氧自由基和脂质过氧化的重要性最终取决于能否更清楚地证明，早期应用有效的抗自由基或抗过氧化剂可促进人类中枢神经系统损伤后的存活和神经功能恢复。
