Funata N, Okeda R, Takano T, Miyazaki Y, Higashino F, Yokoyama K, Manabe M
Acta Pathol Jpn. 1982 Mar;32(2):219-29. doi: 10.1111/j.1440-1827.1982.tb02043.x.
The cerebral and cerebellar lesions of the cats that were exposed to 0.3% carbon monoxide gas under artificial respiration were examined by an electron microscope at different intervals. During the first few days, the most outstanding features were segmental empty axonal swelling, dilatation of the extracellular space, swelling and necrosis of astrocytes and oligodendroglias, and lamellar separation of the myelin sheath predominantly in the deep cerebral white matter. These changes subsided within one week. Instead, collapsed myelin increased in number and phagocytosis of disintegrated myelin was occasionally observed. Astrocytes and oligodendroglias became prominent in size and number. Changes suggestive of selective damage of myelin or oligodendroglia was not encountered. We proposed that CO-followed by Wallerian degeneration. The pathogenesis of CO-encephalopathy was also discussed.
对在人工呼吸条件下暴露于0.3%一氧化碳气体的猫的大脑和小脑病变，在不同时间间隔用电子显微镜进行了检查。在最初几天，最突出的特征是节段性空泡状轴突肿胀、细胞外间隙扩张、星形胶质细胞和少突胶质细胞肿胀及坏死，以及主要在大脑深部白质的髓鞘板层分离。这些变化在一周内消退。相反，崩解的髓鞘数量增加，偶尔可观察到对崩解髓鞘的吞噬作用。星形胶质细胞和少突胶质细胞在大小和数量上变得突出。未发现提示髓鞘或少突胶质细胞选择性损伤的变化。我们提出一氧化碳中毒继以华勒变性。还讨论了一氧化碳脑病的发病机制。
