Cigarette smoke modifies bleomycin-induced lung injury to produce lung emphysema.
The effect of cigarette smoke exposure on the development of bleomycin (BLM)-induced pulmonary fibrosis was studied. Hamsters 3 weeks of age were divided into four groups, control (C), BLM treated (B), cigarette smoke exposure (T), and cigarette smoke plus BLM (TB). Cigarette smoke exposure was started 5 days after the beginning of feeding in a desiccator which received a flow of smoke. A single intratracheal dose of 0.5 mg of BLM per 100 g body weight was administered 30 days after feeding. Sixty days after feeding the animals were killed for measurement of pressure-volume (P-V) relationships and microscopic observations. At 60 days the deflation P-V curves in B and TB were shifted significantly downward and to the right of that of C and T, respectively. P-V curves in TB were shifted significantly upward and to the left of that of B, almost returning to that of C. Light-microscopic examination showed no evidence of emphysema in the lung of T. In contrast, in the lung of TB there were destruction of the alveolar walls, varying degrees of enlargement of alveolar spaces and fibrous thickening of the alveolar septa. These results suggest that BLM-induced lung injury may be modified by cigarette smoke to produce lung emphysema.
D000818:Animals; D001761:Bleomycin / Q000009:adverse effects*; D006224:Cricetinae; D008297:Male; D008647:Mesocricetus; D010947:Plants, Toxic; D011656:Pulmonary Emphysema / Q000209:etiology* / Q000473:pathology; D011658:Pulmonary Fibrosis / Q000139:chemically induced* / Q000209:etiology / Q000473:pathology; D012906:Smoke / Q000009:adverse effects*; D014026:Nicotiana
D012906:Smoke; D001761:Bleomycin