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作 者:于新[1] 刘宗惠[1] 王亚奇[1] 崔月汉[1] 王晶翼[1] 杨希明[1] 骆训懿[1] 谢邦铁[1] 刘晓林[1]
机构地区:[1]北京市海军总医院全军神经外科中心
出 处:《中华航海医学杂志》1996年第2期88-91,共4页
摘 要:目的:进一步证实氧自由基(OFR)在创伤性脑水肿发生中的作用和外源性超氧化物歧化酶(SOD)的防治作用。方法:用硬膜外自由落体打击致猫重型颅脑损伤,随机分为外伤组、游离SOD(F-SOD)治疗组和脂质体包埋SOD(L-SOD)治疗组。观察伤后1、3、6、24小时动物意识及肢体活动、EEG、血清和CSF中脂质过氧化物(LPO)和SOD含量、24小时后脑含水量、血脑屏障通透性、脑组织脂质过氧化物(LPO)和SOD含量以及组织形态学改变。结果与结论:OFR是脑外伤后继发性脑损伤和脑水肿的重要因素之一;外源性F-SOD和L-SOD均对创伤性脑水肿有防治作用,但后者作用更显著。Aim:To verify the role of oxygen free radicals (OFR)in traumatic brain edema and the preventive effect of SOD. Methods:An animal model of severe traumatic brain edema induced by ex-tradural impact was established in cat.Then the animals were randomly divided into three groups,namely the jnjury group,the free-SOD(F-SOD)treated group and the liposome entrapped SOD( L-SOD)treated group (the latter 2 groups were given intravenous injection of F-SOD and L-SOD 50 000U/kg immediatly after the injury respectively).The observation parameters included conciousness score,EEG, lipid peroxides(LPO)and SOD in serum and cerebrospinal fluid at 1,3,6,24 hours after the injury,the brain water content,blood brain barrier(BBB)permeability,the LPO and SOD contents and pathological changes of the brain tissue at 24 hours after the injury. Results and conclusion:OFR is one of the main factors inducing the delayed development of traumatic brain edema and that both F-SOD and L-SOD have preventive effect against the edema,of which the latter is mOre effective,(Fig 5-1~2 inside back cover page)
分 类 号:R742.7[医药卫生—神经病学与精神病学] R977.3[医药卫生—临床医学]
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