大鼠急性一氧化碳中毒后迟发性脑病模型的建立

Establishment of delayed neuropsychologic sequelae rat model after acute carbon monoxide poisoning

目的:建立大鼠急性一氧化碳(CO)中毒致迟发性脑病模型,以探讨其发病机制.方法:质量240～280g雄性SD大鼠,于动物实验高压氧舱内行急性CO暴露,以Morris水迷宫中搜索目标的逃避潜伏期(escapelatency)来评价大鼠的认知记忆能力,并于染毒后3,7,10,20d取脑组织,常规制备石蜡病理切片,行HE染色观察急性CO中毒后大鼠脑皮质及海马神经元的病理性改变.结果:大鼠在2000×10-6体积分数CO浓度和3000×10-6体积分数CO浓度下分别暴露40min和20min后全部昏迷,Morris水迷宫测试发现CO暴露组大鼠逃避潜伏期显著落后于空气对照组(F=4.74,P=0.047),病理学检查发现CO暴露组大鼠的皮质及海马有明显的神经元变性坏死.结论:本实验建立的模型基本模拟了CO中毒后迟发性脑病患者中枢神经系统损伤的行为学特征改变,且有相应的病理学检测结果作为其佐证.

AIM： To establish the delayed neuropsychologic sequelae rat model after acute carbon monoxide （ CO ） poisoning for further elucidating its pathogenesis. METHODS： Male SD rats （240 -280 g BW） were poisoned with CO in the animal experimental hyperbaric oxygen chamber. Cognitive ability was measured by the escape latency of searching the objective in the Morris water maze. The brains of the rats （3, 7, 10, 20 d after poisoning） were taken for paraffin pathological section and HE staining to observe the pathological change in cerebral cortex and hippocampal area. RESULTS ： Rats lost consciousness when they were exposed to 2000 ppm （part per million） CO for40 min and then 3000 ppm for up to 20 rain. Maze test showed that the escape latency of the CO poisoned rats was significantly longer than the air exposed rats （ F = 4.74, P = 0. 047）. The pathological examination revealed apparent neuronal degeneration and necrosis in the cerebral cortex and hippocampal area in CO poisoned rats. CONCLUSION： Besides the evidence of pathologic results, our models basically simulate the praxiologic change induced by central nervous system damage in the patients with delayed neuropsychologic sequelae after CO poisoning.