Smoke inhalation injury and the effect of carbon monoxide in the sheep model.
The role of carbon monoxide (CO) in causing the physiologic and anatomic changes characteristic of smoke inhalation injury was evaluated in 34 sheep. The smoke-exposed group received a dose of smoke known to produce mild inhalation injury. The CO group received a pure gas mixture that contained concentrations of oxygen, carbon dioxide, and CO similar to those in the smoke. Cardiopulmonary function was measured immediately after exposure, and 24 and 72 hours after exposure. The CO group showed a transient increase in cardiac output, but the smoke group showed no such response. The CO group maintained normal PaO2 levels during the 72-hour study period; the smoke group gradually developed hypoxemia. The lungs of the CO exposed animals had no discernible histologic changes; lungs of the smoke group showed progressive inflammatory changes. These results indicate that CO per se is not the primary etiologic agent of smoke inhalation injury.
Shimazu
T
T
U.S. Army Institute of Surgical Research, Fort Sam Houston, Texas 78234-5012.
Ikeuchi
H
H
Hubbard
G B
GB
Langlinais
P C
PC
Mason
A D
AD
Pruitt
B A
BA
D000818:Animals; D002248:Carbon Monoxide / Q000633:toxicity*; D002263:Carboxyhemoglobin / Q000032:analysis; D002302:Cardiac Output; D008168:Lung / Q000648:ultrastructure; D008297:Male; D008855:Microscopy, Electron, Scanning; D010100:Oxygen / Q000097:blood; D012756:Sheep; D015208:Smoke Inhalation Injury / Q000097:blood / Q000473:pathology / Q000503:physiopathology*; D014655:Vascular Resistance
D002248:Carbon Monoxide; D002263:Carboxyhemoglobin; D010100:Oxygen