Shuaib A, Breker-Klassen M M
Department of Medicine (Neurology), College of Medicine, University of Saskatchewan, Saskatoon, Canada.
Neurosci Biobehav Rev. 1997 Mar;21(2):219-26. doi: 10.1016/s0149-7634(96)00012-7.
Cessation of cerebral blood flow results in severe damage to neurons and other brain structures. This is secondary to a combination of energy loss, excessive excitation promoting intracellular Ca2+ buildup, relative lack of inhibitory responses, generation of oxygen free radicals, especially during the reperfusion period and several other destructive cascades. Therapies aimed at decreasing the ill effects of glutamate are either not effective or have serious side-effects. Ca2+ entry blockers are generally not effective in cerebral ischemia, and data with protective effects of oxygen free radical scavengers in the post-ischemic period have shown conflicting results. There is recent interest with the use of agents that increase cerebral inhibitory responses after an ischemic insult. Such agents are effective when used before, during or up to 4 h after the ischemic insult. Many such medications have few side-effects and are in clinical use for other indications. This review will summarize inhibitory mechanisms that may be important in cerebral ischemia, and provide experimental evidence for their potential efficacy.
脑血流停止会导致神经元和其他脑结构严重受损。这继发于能量丧失、过度兴奋促使细胞内钙离子蓄积、相对缺乏抑制性反应、氧自由基生成（尤其是在再灌注期）以及其他几种破坏性级联反应的综合作用。旨在减轻谷氨酸不良影响的疗法要么无效，要么有严重的副作用。钙离子进入阻滞剂在脑缺血中通常无效，且关于氧自由基清除剂在缺血后时期具有保护作用的数据显示出相互矛盾的结果。最近人们对使用在缺血性损伤后增加脑抑制性反应的药物产生了兴趣。这类药物在缺血性损伤前、期间或损伤后长达4小时使用时是有效的。许多此类药物副作用很少，并且已在临床上用于其他适应症。本综述将总结在脑缺血中可能重要的抑制机制，并为其潜在疗效提供实验证据。
