Acute respiratory failure induced by bleomycin and hyperoxia: pulmonary edema, cell kinetics, and morphology.
The acute manifestations of experimental bleomycin- and hyperoxia-induced lung damage were examined. Hamsters were treated with 5 U/kg bleomycin intratracheally followed by exposure to 80% oxygen (O2). As little as 12 hr of O2 exposure potentiated the bleomycin injury; however, the onset of mortality was 72 hr after treatment. The onset of pulmonary edema, measured by radiolabeled tracers, also occurred 72 hr after treatment. Cell kinetics studies showed that 24 hr exposure to 80% O2 did not alter early alveolar cell proliferation. Treatment with bleomycin alone did result in an early increase in alveolar macrophage and type II pneumocyte labeling. Animals treated with both bleomycin and hyperoxia had an increase in macrophage labeling, but not in type II pneumocyte labeling. We conclude that increased macrophage numbers associated with suppressed type II pneumocyte proliferation may play key roles in the potentiation and development of lung damage caused by bleomycin and hyperoxia treatment.
D000818:Animals; D001345:Autoradiography; D001761:Bleomycin / Q000633:toxicity*; D002453:Cell Cycle; D006224:Cricetinae; D008297:Male; D008647:Mesocricetus; D010100:Oxygen / Q000633:toxicity*; D011650:Pulmonary Alveoli / Q000473:pathology; D011654:Pulmonary Edema / Q000139:chemically induced*; D012131:Respiratory Insufficiency / Q000139:chemically induced*
D001761:Bleomycin; D010100:Oxygen