家兔急性CO中毒迟发性脑病血清SOD活性与MDA含量及质子磁共振波谱分析  

Changes of oxidative stress indices and1H-magnetic resonance spectroscopy in rabbits with delayed encephalopathy after acute carbon monoxide poisoning

作　　者：管叶明[1,2] 刘学春[1,2] 汪青松[1,2] 

机构地区：[1]安徽医科大学解放军临床学院 [2]解放军第105医院神经内科,安徽合肥230031

出　　处：《中国工业医学杂志》2010年第2期92-94,共3页Chinese Journal of Industrial Medicine

基　　金：全军十一五医药卫生科研基金(06H009);南京军区医药卫生科研基金(06MA51)

摘　　要：目的观察家兔急性一氧化碳中毒后迟发性脑病(DNS)血清超氧化物歧化酶(SOD)活性和丙二醛(MDA)水平以及质子磁共振波谱(1H-MRS)各参数的变化,探讨DNS的可能发病机制。方法通过腹腔注射CO制备急性CO中毒迟发性脑病动物模型,对照组和DNS组分别进行1H-MRS检查及血清SOD活性和MDA水平的检测。结果与对照组相比,DNS组额叶及颞叶海马CA1区NAA/Cr较正常对照组显著下降,Cho/Cr及Lac/Cr显著升高;DNS组血清SOD活性明显降低,MDA水平明显升高。结论自由基参与了DNS的发病,可能通过损伤神经元膜结构和功能引起脑内NAA、Cho、Lac含量的变化。Objectives To observe the changes of superoxide dismutase （SOD） activity, malondialdehyde （MDA） level in serum and the coefficients of 1H-magnetic resonance spectroscopy （1H-MRS） in rabbits with delayed encephalopathy after acute carbon monoxide （CO） poisoning for exploring the possible pathogenesis of the delayed encephalopathy caused by CO poisoning. Methods The animal model of delayed encephalopathy after carbon monoxide poisoning was established by injection of high-dose CO intraperitoneally in rabbits, then detected the SOD activities and MDA levels in serum of the rabbits, meanwhile, the coefficients of 1H-MRS were also measured. Results The results showed that the ratio of NAA /Cr in frontal lobe and hippocampus CA1 area by 1H-MRS, as well as the serum SOD activity were significantly decreased in the CO injected group, while the ratios of Cho/ Cr, Lac/ Cr and serum MDA levels were remarkably increased compared with control group. Conclusions The results suggested that free radical could be one of the main causes induced delayed encephalopathy after acute CO poisoning, which might damage the function and membrane structure of neuron.

关 键 词：急性一氧化碳中毒 迟发性脑病 磁共振波谱 超氧化物歧化酶(SOD) 丙二醛(MDA) 

分 类 号：R135.14[医药卫生—劳动卫生]