Ando Y, Inoue M, Hirota M, Morino Y, Araki S
Department of Biochemistry, Kumamoto University Medical School, Japan.
Brain Res. 1989 Jan 16;477(1-2):286-91. doi: 10.1016/0006-8993(89)91416-9.
Although the involvement of reactive oxygen species has been suggested in the pathogenesis of brain edema, direct evidence supporting this concept is lacking. To elucidate a critical role of oxygen radicals, effect of a superoxide dismutase (SOD) derivative that circulated bound to albumin with a half-life of 6 h on the occurrence of cold-induced brain edema was studied in the rat. When animals were challenged with brain injury by applying a liquid-nitrogen-cold probe to one side of the cerebral hemisphere over the bony skull for 20 s, the vascular permeability of the underlying tissue increased significantly and unilateral brain edema occurred as determined by the accumulation of intravenously injected Evan's blue and the increase in brain weight. Intravenous administration of the SOD derivative markedly suppressed the increase in vascular permeability and the occurrence of brain edema, particularly at their early stages. These and other results suggest that superoxide anion and/or its metabolite(s) might play a critical role in the pathogenesis of traumatic brain injury.
尽管活性氧物质参与脑水肿发病机制的观点已被提出，但支持这一概念的直接证据仍然缺乏。为了阐明氧自由基的关键作用，研究了一种与白蛋白结合循环、半衰期为6小时的超氧化物歧化酶（SOD）衍生物对大鼠冷诱导脑水肿发生的影响。当通过在颅骨上方的一侧大脑半球应用液氮冷探头20秒对动物造成脑损伤时，通过静脉注射伊文思蓝的蓄积和脑重量的增加确定，下层组织的血管通透性显著增加，单侧脑水肿发生。静脉注射SOD衍生物显著抑制了血管通透性的增加和脑水肿的发生，尤其是在早期阶段。这些及其他结果表明，超氧阴离子和/或其代谢产物可能在创伤性脑损伤的发病机制中起关键作用。
