PATHOLOGICAL-CHANGES IN RAT LUNGS FOLLOWING ACUTE SULFUR MUSTARD INHALATION

Citation
Dr. Anderson et al., PATHOLOGICAL-CHANGES IN RAT LUNGS FOLLOWING ACUTE SULFUR MUSTARD INHALATION, Inhalation toxicology, 8(3), 1996, pp. 285-297
Citations number
14
Categorie Soggetti
Toxicology
Journal title
ISSN journal
08958378
Volume
8
Issue
3
Year of publication
1996
Pages
285 - 297
Database
ISI
SICI code
0895-8378(1996)8:3<285:PIRLFA>2.0.ZU;2-B
Abstract
Although the majority of deaths resulting from exposure to sulfur must ard (HD) have been due to pulmonary dysfunction, there are no detailed accounts of the pathogenesis or HD-induced lesions in the respiratory tract. Accordingly, we investigated the early changes within the trac hea and lungs of rats following inhalation exposure to HD. Anesthetize d rats were exposed by intratracheal intubation to vaporized HD (0.35 mg in 100 mu l absolute ethanol) or ethanol alone for 50 min. Animals were euthanatized at 0, 1, 4, 6, 12, 18, and 24 h postexposure (PE), a nd their respiratory tracts were prepared for histological and ultrast ructural examination. In rats exposed to HD, multifocal, petechial hem orrhages were grossly evident on the pleural surface of the lung at 6 h PE. Atelectasis and edema of the accessory lobe occurred at 12-18 h PE. Histologically, lesions in the respiratory tract were confined pri marily to the trachea, bronchi and larger bronchioles. In HD-exposed r ats, there was a progressive depletion of the bronchiolar-associated l ymphoid tissue (BALT), with necrosis of the lymphoid cells as early as 12 h PE. Necrosis and sloughing of tile tracheal and bronchial epithe lia at 6-12 h PE was followed by the formation of fibrinous pseudomemb ranes within the bronchi. Necrosis and separation of airway epithelia occurred at the mucosal/submucosal interface. Pseudomembranes formed a lmost exclusively in deepithelialized areas overlying the BALT. Cartil aginous lesions, characterized by necrosis of individual chondrocytes, were evident at 12 h PE. Pulmonary edema and occasional alveolar hemo rrhage occurred from 18 to 24 h PE. Small bronchioles and alveoli were relatively unaffected and only a few inflammatory cells were observed at any time.