Pulmonary injury in rats following continuous exposure to 60% O2 for 7 days.
Morphological, biochemical, and physiological studies were done on rats exposed to 60% O2 for 7 days. This exposure did not induce O2 tolerance but instead caused a significant decrease in survival time of animals subsequently exposed to pure O2. The activity of lung superoxide dismutases and glucose-6-phosphate dehydrogenase were unchanged after exposure to 60% O2. A decrease in lung compliance was suggested by changes in the total lung capacity and in the pressure-volume curves of excised lungs. Ventilation of these animals with large tidal excursion resulted in pulmonary edema. Morphometric analyses revealed a significant decrease in alveolar air volume and an increase in the number of alveolar macrophages. The most significant lesions involved the pulmonary vascular bed. The volume and thickness of the capillary endothelium was decreased. There were focal areas of pericapillary fluid accumulations, and a number of the smaller vessels had perivascular edema. These findings suggest that significant pulmonary injury occurs in rats exposed to 60% O2 and that the primary site of injury is the pulmonary capillary endothelium.
D000818:Animals; D002196:Capillaries / Q000187:drug effects; D005954:Glucosephosphate Dehydrogenase / Q000378:metabolism; D008168:Lung / Q000098:blood supply / Q000187:drug effects* / Q000201:enzymology; D008176:Lung Volume Measurements; D008297:Male; D010100:Oxygen / Q000633:toxicity*; D011650:Pulmonary Alveoli / Q000187:drug effects; D051381:Rats; D013047:Specific Pathogen-Free Organisms; D013482:Superoxide Dismutase / Q000378:metabolism
D005954:Glucosephosphate Dehydrogenase; D013482:Superoxide Dismutase; D010100:Oxygen