摘 要: 目的 与全脑缺血再灌注模型比较,探讨急性CO中毒大鼠血液循环功能变化特征及其在急性CO中毒迟发性脑病(DECAMP)中的意义。方法 分别采用腹腔注射CO法、Pulsinelli-Brierley方法制备急性CO中毒模型和全脑缺血再灌注模型,观察大鼠血液流变学指标和凝血功能变化特征。结果 全脑缺血再灌注模型迅速出现循环红细胞压积、血浆黏度、全血黏度分别增加约10%、33%和50%,血液凝固性增强,表现为凝血酶原活动度(PTA)增加约35%、凝血酶原时间(PT)和部分凝血活酶时间(APTT)缩短至6.23 s 和10.36 s ,纤维蛋白原(Fib)浓度则增加1.43倍(均与对照组相比)。急性CO中毒模型早期可见全血黏度、红细胞压积均约降低25%,取血后4 h仍未见血液凝固,亦未检测到Fib,末次染毒1 d后上述观测指标开始逐渐出现逆转,缓慢而隐匿;7~14 d后,PTA较对照组增加约1.20倍,PT和APTT分别较对照组约缩短27%和29%,Fib浓度逐渐增加,7~14 d时达高峰,为对照组的1.50倍。结论 急性CO中毒可诱发持续性微循环异常,早期为凝血功能减退,血液稀释,待血中CO排出后(末次注射CO一天后),则出现血液浓缩、凝血功能大幅增强改变,成为诱发脑内微血栓形成重要的生化基础,此变化可能是CO中毒后发生迟发性脑病的关键环节,对探究DECAMP的分子机制及早期诊断、有效防治具有重要理论价值。 |
关键词: 急性一氧化碳中毒 迟发性脑病 脑循环,血液流变学 |
中图分类号: R595.1
文献标识码:
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基金项目: 国家自然科学基金(细胞外组蛋白介导血小板聚集引起的循环障碍对急性CO中毒迟发性脑病的致病作用研究,批准号:81541161) |
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Study on feature of cerebral circulation after acute carbon monoxide poisoning in rats |
Guan Li, Zhao Jinyuan, Mao LiJun, Zhang Yanlin
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Research Center of Occupational Medicine, The Third Hospital of Peking University,Beijing 100191, China
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Abstract: Objective Compared with the model of ischemia-reperfusion, further investigate the feature of cerebral circulation and its role played in the pathogenesis of delayed encephalopathy after acute carbon monoxide poisoning(DECAMP). Methods The ischemia-reperfusion model and acute CO poisoning model were established by Pulsinelli-Brierley method, and CO-injection i.p, respectively, compare the changes and features of erebral circulation. Results The results showed that comparlng with the control group, the hematocrit (HCT), whole blood viscosity and plasma viscosity were increased about 10%, 33% and 50% respectively, the prothrombin activity (PTA) increased by 35%, prothrombin time (PT) and partial thromboplastin time (APTT) shortened to 6.23s and 10.36s respectively, fibrinogen (Fib) concentration was increased of 1.43 times in ischemia-reperfusion group. While in CO poisoning, at the early stage the HCT and the whole blood viscosity even decreased by 25% compared with control group, and the Fib in plasma could be not detected, too; but one day later after CO injection, all the indices mentioned above were all reversed,7 days after CO injection, the blood showed a gradually enhanced hypercoagulative state :compared to the control group,PTA had 1.20 times increase, PT and APTT were shortened by 27% and 29% respectively, plasma Fib level also rised 1.5 times. Conclusion The results suggested that acute CO poisoning might induce a sustained cerebral circulation dysfunction, there were coagulation dysfunction and blood dilution at the early stage of CO poisoning, and blood concentration, high blood viscosity and hyper-coagulation in cerebral circulation when CO was completely discharged (one day later after last injection of CO), which should be important biochemical basis to induce cerebral micro-thrombosis, and key link of the pathogenesis of DECAMP, which would play a irreplaceable role in the study of molecular mechanism, early diagnosis and effective therapy on DECAMP . |
Keywords: acute carbon monoxide poisoning delayed encephalopathy cerebral circulation, hemorheology |