Related Experiment Video
Updated: Aug 10, 2026

Bilateral Common Carotid Artery Occlusion as an Adequate Preconditioning Stimulus to Induce Early Ischemic Tolerance to Focal Cerebral Ischemia
Published on: May 9, 2013
Prolonged exposure to one percent carbon monoxide causes a leucoencephalopathy in un-anaesthetised sheep
D F Gorman1, Y L Huang, C Williams
1Department of Medicine, Faculty of Medical and Health Sciences, University of Auckland, Private Bag 92019, Auckland, New Zealand. d.gorman@aukland.ac.nz
Abstract:
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.

