中文摘要：

目的 探讨急性一氧化碳（CO）中毒后大鼠血液流变学及凝血功能变化的特点及其在急性CO中毒迟发性脑病（DNS）中的作用.方法 采用腹腔注射CO法制备急性CO中毒大鼠模型;采用Pulsinelli-Brierley方法制备全脑缺血再灌注大鼠模型,根据神经病理学检查和Morris水迷宫行为学试验鉴定大鼠是否发生DNS,并进一步观察出现脑病大鼠的血液流变学变化特征.结果 全脑缺血再灌注模型大鼠在再灌注后很快出现血细胞比容、血浆黏度及全血黏度明显增加血液流变学异常和血液凝固性增强等凝血功能障碍;急性CO中毒DNS模型大鼠早期可见红细胞变形指数降低（36.717±1.818）,且全血黏度、血细胞比容（29.65±0.61）亦均降低的血液流变学改变,同时凝血功能明显下降,此间未见明显的循环功能障碍.在末次染毒1 d后上述指标开始向全脑缺血再灌注模型表现转变,7～14 d后达到高峰,但不及缺血再灌注组变化剧烈.结论 急性CO中毒后可诱发微循环障碍,且具有与其他原因所致循环障碍不同的特点,此变化可能是CO中毒后发生DNS的重要病理学基础.

英文摘要：

Objective To investigate the startup detail of circulation dysfunction and its role in the progress of delayed neuropsychologic sequelae（DNS）after carbon monoxide（CO）poisoning with comparison with the model of ischemia-reperfusion.Methods The ischemia-reperfusion rat model was established by Pulsinelli-Brierley method, and the CO poisoning rats model by i.p.injected with CO repeatedly respectively,and the rats were identified with DNS following the experiment of pathology and the ethnology.Results The whole blood viscosity, plasma viscosity, hematocrit and fibrinogen increased significantly immediately after reperfusion, and recovered gradually with the ischemia-reperfusion rat model.The whole blood viscosity decreased significantly immediately after CO treated i.p.Especially at low shear rate, the hematocrit also declined remarkably in the early stage after CO treatment.But 1day later, these parameters turned to the trend of the ischemia-reperfusion rats.There was a prominent elevation of both indexes until the 14th day following CO injection i.p.Conclusion There are significantly sustained hyper-coagulation and hyper-viscosity with circulation in rats after CO poisoning compared with ischemia-reperfusion model during the period of DNS, which might contribute to increase cerebral circulation resistance, blocked blood flow, and deteriorate hypoxemia in progression of DNS.