Morphologic and physiologic response of lungs to steroid and cigarette smoke: an animal model.
The combined effects of cigarette smoke inhalation and hydrocortisone acetate (HCA) treatment induce prominent abnormalities in lungs of C57BL/6 male mice. These abnormalities include (1) a marked reduction of pulmonary macrophage population which is normally elevated by smoke inhalation, (2) an accumulation of surfactant and flocculent material in alveoli, (3) a decrease in alveolar space surrounded by normal septal tissue, and (4) an increase in hypertrophied alveolar parenchyma. Concomitant with altered lung morphology, lung volume and gas diffusing capacity were significantly compromised in animals subjected to smoke exposure and steroid treatment. It was found that smoke inhalation or HCA administration alone had no ill effects on the animals. The data presented indicate that manifestation of pathologic conditions resembling pulmonary fibrosis and pulmonary alveolar proteinosis is a result of cigarette smoke-drug interaction. The information reported provides a basis for an animal model which might be applicable to assessment of factors related to smoke inhalation and development of pulmonary disorders.
D000818:Animals; D006854:Hydrocortisone / Q000031:analogs & derivatives* / Q000633:toxicity; D008168:Lung / Q000187:drug effects / Q000473:pathology*; D008264:Macrophages / Q000648:ultrastructure; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008954:Models, Biological; D010947:Plants, Toxic; D011650:Pulmonary Alveoli / Q000473:pathology; D012906:Smoke / Q000009:adverse effects*; D014026:Nicotiana; D014109:Total Lung Capacity
D012906:Smoke; C021650:hydrocortisone acetate; D006854:Hydrocortisone