CAJ | 학술논문

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.
목적 탐토급성일양화탄(CO)중독후대서혈액류변학급응혈공능변화적특점급기재급성CO중독지발성뇌병(DNS)중적작용.방법 채용복강주사CO법제비급성CO중독대서모형;채용Pulsinelli-Brierley방법제비전뇌결혈재관주대서모형,근거신경병이학검사화Morris수미궁행위학시험감정대서시부발생DNS,병진일보관찰출현뇌병대서적혈액류변학변화특정.결과 전뇌결혈재관주모형대서재재관주후흔쾌출현혈세포비용、혈장점도급전혈점도명현증가혈액류변학이상화혈액응고성증강등응혈공능장애;급성CO중독DNS모형대서조기가견홍세포변형지수강저(36.717±1.818),차전혈점도、혈세포비용(29.65±0.61)역균강저적혈액류변학개변,동시응혈공능명현하강,차간미견명현적순배공능장애.재말차염독1 d후상술지표개시향전뇌결혈재관주모형표현전변,7～14 d후체도고봉,단불급결혈재관주조변화극렬.결론 급성CO중독후가유발미순배장애,차구유여기타원인소치순배장애불동적특점,차변화가능시CO중독후발생DNS적중요병이학기출.
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.