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The pathophysiology of carbon monoxide poisoning and acute respiratory failure in a sheep model with smoke inhalation injury.

Abstract
A smoke inhalation model was created in 22 adult male sheep with pine smoke inhalation through an endotracheal tube for 6 min. Arterial blood gases, HbCO, HbO2 and pulmonary compliance (Cdyn) were monitored, and the morphology of the tracheobronchial tree and pulmonary parenchyma were studied by light and electron microscopy. Severe carbon monoxide poisoning with fatal levels of HbCO (greater than 50 percent) was found at the end of smoke inhalation. Acute respiratory distress, progressive hypoxemia, decreased pulmonary compliance and increased P(A-a)O2 and Qs/QT occurred after injury. Tracheobronchial blockade by pseudomembrane cast, pulmonary edema, atelectasis and necrosis of pulmonary epithelia were demonstrated pathologically. The mechanisms of CO poisoning and ARF are discussed.
AuthorsC Z Wang, A Li, Z C Yang
JournalChest (Chest) Vol. 97 Issue 3 Pg. 736-42 (Mar 1990) ISSN: 0012-3692 [Print] United States
PMID2306976 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Carbon Monoxide
  • Oxygen
Topics
  • Acute Disease
  • Animals
  • Bronchi (pathology)
  • Carbon Monoxide (blood)
  • Carbon Monoxide Poisoning (etiology, pathology, physiopathology)
  • Disease Models, Animal
  • Lung (pathology)
  • Male
  • Oxygen (blood)
  • Pulmonary Edema (etiology, pathology)
  • Pulmonary Gas Exchange (physiology)
  • Respiration (physiology)
  • Respiratory Insufficiency (etiology, pathology, physiopathology)
  • Sheep
  • Smoke Inhalation Injury (complications, pathology, physiopathology)
  • Trachea (pathology)

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