Acute carbon monoxide poisoning in an animal model: the effects of altered glucose on morbidity and mortality.
An animal model in which the common carotid artery and the jugular vein serving one side of the brain are occluded by indwelling catheters has been used during the past few years to investigate acute carbon monoxide (CO) poisoning. This article reviews the recent research examining the pattern of changes in blood glucose concentration which results from CO exposure, and the manner in which altered glucose concentration alters neurologic outcome and mortality. At present it appears that either greatly depressed glucose or greatly elevated glucose during and/or after CO exposure increases morbidity and mortality. Cyanide (CN) poisoning, in contrast to CO, produces a different pattern of changes in blood glucose and lactate, and unlike CO, fails to slow cardiac AV conduction and ventricular repolarization. Through the use of magnetic resonance imaging and spectroscopic techniques, cerebral cortical edema and the changes in brain phosphagens have been assessed following CO poisoning in the rat. The published results as well as data from recent pilot studies are discussed in the light of our current understanding of CO toxicology.
Penney
D G
DG
Department of Physiology, Wayne State University School of Medicine, Detroit, MI 48201.
D000818:Animals; D002249:Carbon Monoxide Poisoning / Q000453:epidemiology / Q000378:metabolism* / Q000401:mortality; D004195:Disease Models, Animal; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D009017:Morbidity; D051381:Rats; D017207:Rats, Sprague-Dawley; D012966:Sodium Cyanide / Q000506:poisoning
D005947:Glucose; D012966:Sodium Cyanide