Zhongguo wei zhong bing ji jiu yi xue = Chinese critical care medicine = Zhongguo weizhongbing jijiuyixue · 2004
[Intoxication induced by unsymmetrical dimethylhydrazine: characteristics and mechanism of its acute and chronic injuries].
Аннотация на английскомСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Yue Mao-xing, Peng Rui-yun, Wang Zheng-guo, Wang De-wen, Yang Zhi-huan, Yang He-ming, Su Qun, Xia Ya-dong, Gao Ya-bing, Cui Xue-mei, Li Jian-zhong, Li Yan
Аннотация
OBJECTIVE: To investigate the characteristics and mechanism of the acute and chronic injuries induced by unsymmetrical dimethylhydrazine (UDMH).
METHODS: A total of 128 male rats were randomly divided into four groups: UDMH intoxication acute response group and chronic response group, and corresponding control groups. UDMH was administrated through inhalation at the concentration of 8x10(-4)g/m(3) for 15 minutes. Animals of each group were sacrificed at 3, 6, 12, 24, 48 and 72 hours respectively after the intoxication. Pathologic changes and blood gas were examined. Chronic injuries and pathologic changes were also observed 1 year after the intoxication.
RESULTS: Major pathological changes in the intoxication group were cerebral edema, degeneration and necrosis of neuron, enlargement and hemorrhage of capillary. Damages of different degree were found in liver, kidney, lung, heart, spleen, stomach, intestine, thymus, blood, bone marrow. Pallium ischemia was also found in the intoxicated rats 1 year after the intoxication, including ischemia damage of neuron in cerebral cortex, hemorrhage and focal liquefaction of thalamus and medulla conducting bind, dissociation, rupture, not uniform circuitry in conducting fibers.
CONCLUSION: Our study reveals the basic pathological induced by intoxication of UDMH. The most severe stage of the injury appears 2-6 hours after intoxication. Long term investigation reveals pallium ischemia, thalamus hemorrhage and liquefaction in the medulla oblongata 1 year after the intoxication with UDMH. All the changes are significant.
METHODS: A total of 128 male rats were randomly divided into four groups: UDMH intoxication acute response group and chronic response group, and corresponding control groups. UDMH was administrated through inhalation at the concentration of 8x10(-4)g/m(3) for 15 minutes. Animals of each group were sacrificed at 3, 6, 12, 24, 48 and 72 hours respectively after the intoxication. Pathologic changes and blood gas were examined. Chronic injuries and pathologic changes were also observed 1 year after the intoxication.
RESULTS: Major pathological changes in the intoxication group were cerebral edema, degeneration and necrosis of neuron, enlargement and hemorrhage of capillary. Damages of different degree were found in liver, kidney, lung, heart, spleen, stomach, intestine, thymus, blood, bone marrow. Pallium ischemia was also found in the intoxicated rats 1 year after the intoxication, including ischemia damage of neuron in cerebral cortex, hemorrhage and focal liquefaction of thalamus and medulla conducting bind, dissociation, rupture, not uniform circuitry in conducting fibers.
CONCLUSION: Our study reveals the basic pathological induced by intoxication of UDMH. The most severe stage of the injury appears 2-6 hours after intoxication. Long term investigation reveals pallium ischemia, thalamus hemorrhage and liquefaction in the medulla oblongata 1 year after the intoxication with UDMH. All the changes are significant.