一氧化碳中毒所致小鼠迟发性脑病的病理变化及机制

Pathological changes and mechanism of delayed encephalopathy in mice induced by carbon monoxide poisoning

【目的】探讨小鼠一氧化碳中毒所致迟发性脑病大脑、脊髓、周围神经的病理变化及其发病机制。【方法】将小鼠随机分为2组:A组(8只),空气(100ml/kg)腹腔注射1次/d,连续7d;B组(20只)CO(100ml/kg)腹腔注射1次/d,连续7d。观察实验动物神经系统表现,分别于1、2、3、4周取大脑、小脑、脊髓、周围神经多聚甲醛固定,KB、GFAP、ED1、MBP染色观察。电镜观察神经组织超微结构病理改变。【结果】迟发性脑病小鼠多在中毒后7d表现为精神萎靡、运动迟滞、活动减少等。组织病理学显示:中毒后1周海马神经元、小脑浦肯野细胞数量减少,大脑皮层神经元变性、数量减少,脑组织内小血管扩张、数量增多。第2~3周皮层神经元仍见到变性坏死,明显的胶质细胞反应。大脑及小脑白质结构疏松,KB染色可见到明显的髓鞘脱失,尤其是以胼胝体、视束损害明显。脊髓前外侧区可见到细胞变性。电镜可见第2周开始海马神经元出现核固缩、核碎裂,细胞凋亡。【结论】一氧化碳中毒所致小鼠迟发性脑病发病机制包括后期的细胞凋亡及炎症反应的发生。

[Objective]To explore the Pathological changes and mechanism of cerebrum, spinal cord, and peripheral nerve in mice with delayed encephalopathy caused by carbon monoxide poisoning（DEACMP）. [ Methods] Mice were randomly divided into 2 groups： group A （8） and group B （20）. Both groups were intraperitoneally injected respectively with air （100 ml/kg） and CO （100 ml/kg） once a day for 7 consecutive days. Neurological manifestations were observed. On the 1st, 2nd, 3rd, 4th week cerebrum, cerebellum, spinal cord, and pe- ripheral nerve were fixed with paraformaldehyde and observed through KB, GFAP, ED1, and MBP, and at the same time pathological changes of uhrastructural nervous tissues were observed through electron microscope. [ Results ] Seven days after carbon monoxide poi- soning, mice with delayed encephalopathy showed such performance as listlessness, retardation, reduced activity. Histopathological ob- servation showed： 1 week after poisoning, the nmnber of cells in hippocampal neurons and cerebellar Purkinje decreased, cerebral cor- tex neuron degenerated, and the small blood vessels expanded in the brain tissue rose in Numbers. On the 2nd and 3rd weeks cortical neurons degeneration and necrosis could still be seen, and the glial ceil response could be seen clearly. White matter loose structures could be seen in cerebrum and cerebellum, and demyelination could be clearly seen under KB staining, especially in corpus callosum and optic tract. Cellular degeneration could be seen in the anterolateral area of the spinal cord. From the 2nd week, under electron mi- croscope, nucleus p^cnosis, nuclear fragmentation and cell apoptosis could be seen in hippocampal neurons. [ Conclusion ] Pathological mechanism of DEACMP included apoptosis and inflammation of the nervous system damage.