Cardiovascular, metabolic and neurologic effects of acute carbon monoxide poisoning in the rat.
Acute severe carbon monoxide poisoning was investigated in a modified Levine preparation. The rats inhaled 2700 p.p.m. CO for 90 min (COHb = 80%). Body temperature, heart rate and carotid systemic and 'stump' blood pressure declined sharply during CO exposure. By 2 and 4 h post-CO, body temperature and blood pressure had not renormalized, while heart rate was elevated. Blood glucose was unchanged at termination of CO exposure, but increased from 115 mg/dl to 191 mg/dl by 2 h post-CO. Hematocrit increased significantly during CO exposure, but no change in plasma volume was observed. Many rats showed one-sided muscle weakness and unidirectional rotation. By 4 h post-CO, behaviorally-assessed neurologic deficit was strongly correlated with an increase in left cerebral hemisphere water content, demonstrating a direct relationship between brain edema and dysfunction resulting from CO poisoning.
Penney
D G
DG
Department of Physiology, Wayne State University School of Medicine, Detroit, MI 48201.
Verma
K
K
Hull
J A
JA
D000208:Acute Disease; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D001794:Blood Pressure / Q000187:drug effects; D001831:Body Temperature / Q000187:drug effects; D001929:Brain Edema / Q000139:chemically induced; D002249:Carbon Monoxide Poisoning / Q000150:complications / Q000503:physiopathology*; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D051381:Rats; D011919:Rats, Inbred Strains
D001786:Blood Glucose