The Role of Eicosanoids in a Model of Smoke-Induced Lung Injury
Abstract
Smoke inhalation has been identified as a major cause of lung injury and death in fires with mortality rate of approximately 75%. Soldiers regularly occupy enclosed spaces and travel near flammable fuels. The combination of burning material and an enclosed space are major factors that lead to smoke inhalation. We used a combination of diesel fuel and polycarbonate plastic to generate smoke-induced lung injury. Rabbits were exposed to 60 tidal volume breaths of smoke in approximately 10 minutes. Acute smoke exposure caused changes in broncho-alveolar lavage (BAL) and plasma eicosanoid concentration, especially at 0.5 hours post-smoke exposure. In addition, there were decreases in technetium-labeled diethylene-triamine pentaacetic acid (99mTcDTPA) T1/2, increases in BAL total white cell count and alveolar macrophage acid phosphatase activity, and pathological evidence of pulmonary edema and type 2 pneumocyte injury. We conclude that lung eicosanoids are involved in the inflammatory process caused by severe smoke inhalation. However, the specific roles these lung eicosanoids play in the smoke-induced injury process are not known at this time. Keywords: Smoke exposure, Eicosanoids, Prostaglandins, Leukotrienes, Broncho-alveolar lavage, Alveolar epithelial permeability, Eicosane, Combustion products.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jun 29, 1988
- Accession Number
- ADA199120
Entities
People
- Mark L. Witten
Organizations
- University of Arizona