Gorman D F, Huang Y L, Williams C
Department of Medicine, Faculty of Medical and Health Sciences, University of Auckland, Private Bag 92019, Auckland, New Zealand.
Toxicology. 2001 Aug 28;165(2-3):97-107. doi: 10.1016/s0300-483x(01)00413-9.
A total of 15 Levine-prepared adult un-anaesthetised sheep were exposed to 1% carbon monoxide (CO) in air for between 45 and 150 min. This exposure caused a reversible increase in blood carboxyhaemoglobin concentration and heart rate, and a similarly reversible decrease in electroencephalographic frequency and level of consciousness. sheep were either normotensive or slightly hypertensive. Sheep brains were subsequently examined for histopathological changes at either 5 or 14 days post- exposure. No dead neurons or apoptotic cells were seen, but most sheep given a prolonged exposure to CO had some axonal damage and associated gliosis. This damage was concentrated about necrotic micro-foci in the peri-ventricular white matter. These results suggest that a leucoencephalopathy is a primary consequence of acute and sub-acute CO toxicity.
总共15只按照莱文方法准备的成年未麻醉绵羊暴露于含1%一氧化碳(CO)的空气中45至150分钟。这种暴露导致血液中碳氧血红蛋白浓度和心率可逆性增加,以及脑电图频率和意识水平同样可逆性降低。绵羊血压正常或略高。随后在暴露后5天或14天检查绵羊大脑的组织病理学变化。未发现死亡神经元或凋亡细胞,但大多数长时间暴露于CO的绵羊有一些轴突损伤及相关的胶质细胞增生。这种损伤集中在脑室周围白质的坏死微灶周围。这些结果表明,白质脑病是急性和亚急性CO中毒的主要后果。