| Literature DB >> 7076218 |
D R Thorning, M L Howard, L D Hudson, R L Schumacher.
Abstract
Inhalation of smoke can adversely affect pulmonary function; however, the lack of detailed knowledge of exposure conditions and the overall complexity of ensuing clinical problems generally preclude an understanding of the specific role played by smoke in human victims. Using controlled exposures of rabbits to white pine wood smoke, an animal model of smoke inhalation has been created. Light and electron microscopic examinations of injured respiratory tissues from these animals have revealed a reproducible, necrotizing tracheobronchial epithelial cell injury. By six hours after injury, the epithelium remains largely intact but is infiltrated by inflammatory cells; by 24 hours its ciliated and secretory lining cells are largely destroyed, the inflammatory reaction is maximal, but basal epithelial cells retain their normal structural appearances; by 72 hours, its surfaces are largely covered by a nonciliated, stratified reparative epithelium, apparently derived from proliferating and migrating basal cells. The acute injury and early reactions to injury resemble lesions observed in the lungs of human smoke-injured victims, and suggest several physiologic consequences that would provide likely explanations for some of the disabilities observed in these victims.Entities:
Mesh:
Year: 1982 PMID: 7076218 DOI: 10.1016/s0046-8177(82)80225-6
Source DB: PubMed Journal: Hum Pathol ISSN: 0046-8177 Impact factor: 3.466