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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。
Objective To observe the changes of serum superoxide dismutase (SOD), malondialdehyde (MDA) and proton magnetic resonance spectroscopy (1H-MRS) in delayed encephalopathy (DNS) after acute carbon monoxide poisoning in rabbits. The possible pathogenesis. Methods Animal model of delayed encephalopathy induced by acute CO poisoning was established by intraperitoneal injection of CO. 1H-MRS and serum SOD activity and MDA levels were detected in control group and DNS group respectively. Results Compared with the control group, NAA / Cr in the CA1 area of the frontal lobe and the temporal lobe of DNS group was significantly lower than that of the normal control group, while Cho / Cr and Lac / Cr were significantly increased. Serum SOD activity was significantly decreased and MDA level was significantly increased high. Conclusion Free radicals are involved in the pathogenesis of DNS, which may cause NAA, Cho and Lac changes in the brain through impairing the membrane structure and function of neurons.