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目的:建立可靠的急性一氧化碳(CO)中毒迟发性脑病的动物模型。方法: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;Morris水迷宫检测大鼠1-5w逃避潜伏期;尼氏染色及TUNEL原位末端凋亡染色检测大脑皮质及海马细胞损伤及凋亡。结果:染毒后,大鼠出现典型的CO重度中毒症状,体内血液HbCO浓度迅速升高,使用分次腹腔注射法,大鼠可维持长时间(>12h)高HbCO状态(HbCO>48%);中毒组大鼠水迷宫检测认知功能较对照组下降,病理学检查显示大鼠出现脑细胞损伤、凋亡明显。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,具有简单、可靠、重复性好的特点,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。
Objective: To establish a reliable animal model of delayed encephalopathy after acute carbon monoxide (CO) poisoning. Methods: Male Sprague-Dawley rats were injected intraperitoneally with CO to establish a model to dynamically monitor the concentration of carboxyhemoglobin (HbCO) in the tail blood. The Morris water maze was used to detect the 1-5-day escape latency in rats. Nissl staining and TUNEL in situ end-apoptosis Detection of apoptosis and apoptosis of cerebral cortex and hippocampus by staining of death stain. Results: After exposure to CO, the typical symptom of severe CO poisoning was observed in rats. HbCO concentration in blood rose rapidly. HbCO> 48% was maintained for a long time (> 12h) by using intraperitoneal injection. ; Water maze test rats poisoning group cognitive function decline compared with the control group, pathological examination showed brain injury in rats, the obvious apoptosis. Conclusion: This study established an animal model that is more consistent with the clinical features of delayed encephalopathy, which has the characteristics of simple, reliable and good repeatability, and provides a reliable basis for further study on the mechanism of delayed brain injury induced by acute CO poisoning.