Pulmonary tissue and cigarette smoke. 2. Parenchymal response.
Cigarette smoke and hydrocortisone acetate (HCA) induce marked abnormalities in lungs of C57BL/6J male mice. In many pulmonary regions of smoke-exposed, HCA-treated animals, alveoli were highly congested with surfactant and flocculent material. In addition, prominent alveolar collapse and septal hypertrophy were common. These conditions resembled pulmonary alveolar proteinosis described in humans. Administration of HCA to sham-treated animals also produced lung abnormalities, however, considerably milder in severity, while stress (resulting from sham treatment) or HCA injections of mice alone failed to induce any pulmonary tissue disorder. Data reported indicate that the genesis of abnormal conditions which resemble pulmonary alveolar proteinosis is potentiated by cumulative effects of different treatments (i.e., smoke, HCA, and stress), most significant being the interaction between cigarette smoke and the steroid.
D000818:Animals; D001835:Body Weight; D008168:Lung / Q000473:pathology* / Q000648:ultrastructure; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008854:Microscopy, Electron; D010947:Plants, Toxic; D011650:Pulmonary Alveoli / Q000648:ultrastructure; D012906:Smoke / Q000009:adverse effects*; D014026:Nicotiana
D012906:Smoke