Citation

Gorman D, Drewry A, Huang YL, Sames C. Toxicology 2003; 187(1): 25-38.

Affiliation

Department of Medicine, University of Auckland, Private Bag 92019, Auckland, New Zealand. d.gorman@aukland.ac.nz

Copyright

(Copyright © 2003, Elsevier Publishing)

DOI

unavailable

PMID

12679050

Abstract

Carbon monoxide (CO) is a dangerous exogenous poison and an essential endogenous neurotransmitter. This gas when inhaled has an anaesthetic effect, which is poorly understood, but which may be fatal if compensatory mechanisms are exhausted, if cardiac oxygen (O(2)) needs exceed myocardial oxygenation and/or if apnoea or asphyxia onsets. Although there is considerable evidence that hypoxia occurs late in CO poisoning, both the treatment of acutely poisoned people and environmental exposure limits are largely based on a hypoxic theory of toxicity. The significance of recent demonstrations of increased endogenous CO and NO production in neurons of animals exposed to exogenous CO, and of a related sequestration of leucocytes along the endothelium and subsequent diapedesis is also not fully understood, but may in part explain both acute and delayed deleterious effects of a CO exposure. Delayed brain injuries due to a CO exposure may be preventable by hyperbaric O(2). However, the ideal dose of O(2) in this context, if any, is unknown and other potential treatments need to be tested.

Language: en