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研究目的探讨脂质过氧化作用与急性一氧化碳中毒后迟发性脑病的关系。研究方法疾病组为1991年11月至1992年4月间住院急性一氧化碳中毒后迟发性脑病患者11例,年龄38～80岁;对照组为25例正常人,年龄33～68岁。所有研究对象均抽取空腹静脉血,分离血清,用荧光分光光度法测定过氧化脂质(LPO)和水溶性脂质过氧化物(WSFS)含量,测定结果进行t检验。结果对照组血清LPO和WSFS分别为2.70±0.87μmol/L和16.1±3.8U,疾病组分别为3.64±1.51μmol/L和20.3±3.1U,二项指标疾病组均明显高于对照组(P<0.05,P<0.01)。结论急性一氧化碳中毒后迟发性脑病患者血清LPO及WSFS增高,表明脂质过氧化作用参与了本病的脑组织损伤。
Objective To investigate the relationship between lipid peroxidation and delayed encephalopathy after acute carbon monoxide poisoning. Methods The disease group was 11 patients with delayed encephalopathy after hospitalized with acute carbon monoxide poisoning from November 1991 to April 1992, aged from 38 to 80 years old. The control group was 25 normal people aged from 33 to 68 years. Fasting venous blood was drawn from all the subjects and the serum was separated. The levels of lipid peroxide (LPO) and water-soluble lipid peroxide (WSFS) were determined by fluorescence spectrophotometry. The results were analyzed by t-test. Results The serum levels of LPO and WSFS in the control group were 2.70 ± 0.87μmol / L and 16.1 ± 3.8U, respectively, and were 3.64 ± 1.51μmol / L and 20.3 ± 3.1U in the disease group, and were significantly higher in the bin index disease group than in the control group <0.05, P <0.01). Conclusion Serum LPO and WSFS in patients with delayed encephalopathy after acute carbon monoxide poisoning are increased, indicating that lipid peroxidation is involved in the damage of brain tissue in this disease.