PROTECTIVE EFFECTS OF LIPOSOME-ENTRAPPED SUPEROXIDE-DISMUTASE ON POSTTRAUMATIC BRAIN EDEMA
PROTECTIVE EFFECTS OF LIPOSOME-ENTRAPPED SUPEROXIDE-DISMUTASE ON POSTTRAUMATIC BRAIN EDEMA
复制标题
DOI：
10.1002/ana.410210604
复制
发表时间：
1987-06-01
影响因子：
11.2
通讯作者：
FISHMAN, RA
中科院分区：
文献类型：
--
作者：
CHAN, PH;LONGAR, S;FISHMAN, RA
氧自由基和膜脂质过氧化被认为与继发于缺血和创伤性损伤的脑水肿和细胞死亡有关。使用由冷诱导的损伤引起的脑水肿的模型，我们已经证明了超氧自由基的早期升高，随后在血脑屏障中的渗透性变化和受伤的脑水肿的发展。损伤前5min静脉注射脂质体包埋的铜锌超氧化物歧化酶，促进其进入损伤脑血脑屏障内皮细胞，降低脑内超氧自由基水平，改善血脑屏障通透性改变和脑水肿。伤后5分钟同样治疗也有效。这些数据表明，超氧自由基在脑损伤后血管源性脑水肿的延迟发展中起重要作用。
Oxygen-derived free radicals and membrane lipid peroxidation have been postulated to be involved in brain edema and cell death, secondary to ischemia and traumatic injury. Using a model of brain edema induced by cold-induced injury, we have demonstrated an early elevation of superoxide radicals followed by permeability changes in the blood-brain barrier and development of edema in injured brain. Intravenous injection of liposome-entrapped copper-zinc-superoxide dismutase 5 minutes before the injury-enhanced entry of the enzyme into endothelial cells of the blood-brain barrier of injured brain reduced the brain level of superoxide radicals and ameliorated blood-brain barrier permeability changes and brain edema. Identical treatment 5 minutes after injury was also effective. These data demonstrate that superoxide radicals play an important role in the delayed development of vasogenic brain edema following brain injury.