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迟发性生化改变在中枢神经系统(CNS)创伤性组织损害中起重要作用。这种迟发性损害因素的鉴定,发展了旨在减轻这种进行性组织破坏的各种药物治疗策略。本文着重讨论皮质甾类、抗氧化剂与自由基清除剂、花生四烯酸代谢的调节剂、神经节苷脂、单胺调节剂、阿片受体拮抗剂、促甲状腺激素释放激素(TRH)及其类似物、N—甲基—D—天冬氨酸(NMDA)受体拮抗剂、Ca~(2+)通道拮抗剂和血小板活化因子(PAF)拮抗剂在CNS损伤治疗中的作用及其机理。
Delayed biochemical alterations play an important role in traumatic tissue damage in the central nervous system (CNS). The identification of this late-onset impairment has led to the development of various drug treatment strategies aimed at reducing this progressive tissue destruction. This article focuses on corticosteroids, antioxidants and free radical scavengers, arachidonic acid metabolism regulators, gangliosides, monoamine regulators, opioid receptor antagonists, thyrotropin releasing hormone (TRH) and its Role and Mechanism of Analogs, N-methyl-D-aspartate (NMDA) Receptor Antagonists, Ca 2+ Channel Antagonists and Platelet-Activating Factor (PAF) Antagonists in the Treatment of CNS Injury .