【摘要】 目的　建立急性一氧化碳 (CO)中毒迟发性脑病的动物模型 ,为其机制研究提供基础。方法　体重 2 40～ 2 80g雄性SD大鼠 ,分次腹腔注射CO染毒制备模型 ,动态监测尾血碳氧血红蛋白 (HbCO)浓度 ,确定染毒剂量和间隔。分别于染毒后 1、3、7、14、2 1d取脑组织 ,常规制备石蜡病理切片 ,行HE、Luxol氏坚牢蓝焦油紫及Tunnel原位末端凋亡染色。结果　染毒后 ,大鼠体内血液HbCO迅速升高 ,使用分次腹腔注射法 ,大鼠可维持长时间 (>16h)高HbCO状态 (HbCO >50 % ) ;病理学检查显示染毒大鼠除急性脑损伤外 ,还在染毒 1～ 2周后出现脑细胞凋亡、大脑白质脱髓鞘、大脑基底结区变性坏死等二次损伤改变 ,与临床病理学特点十分吻合。结论　本研究建立了一种较为符合迟发性脑病临床特征的动物模型 ,该模型的建立将可为深入研究急性CO中毒致迟发性脑损伤的机制提供可靠基础更多还原

【Abstract】 ObjectiveTo prepare a convenient and relia bl e animal model of delayed neuropsychologic sequelae (DNS) by acute carbon monoxi de poisoning for exploring its pathogenesis. MethodsMale SD ra ts, BW 240-280 g, were ip injected with CO repeatedly, then dynamically monitor ed the carboxyhemoglobin (HbCO) level in blood for ascertaining the administrati on dose and process. The 1, 3, 7, 14 and 21 days after injection of CO respectiv ely, the brains of the CO exposed rats were taken for pathological section and s taining (HE, LFB and Tunnel stain) respectively. ResultsThe Hb CO levels rised rapidly, being kept at higher level (>50%) for long time (>16h) by the method of repeated injection of CO ip. The pathological examination showe d that except the acute brain damages, there were some delayed pathological chan ges which could be seen one or two weeks after CO injection, such as extensive a poptosis and demyelination in cerebral white matter, degeneration and necrosis i n basal ganglia area etc., which were quite accordant with the clinical features of DNS. ConclusionA new method of preparing DNS animal model caused by acute CO poisoning was established, offering reliable scientific basis for further exploring the pathogenesis of DNS by CO.更多还原