title: Mechanism of pulmonary alveolar injury in experimental Pneumocystis carinii pneumonia in the rat.
abstract: Pneumocystis carinii pneumonia was produced in rats by the administration of corticosteroids and the permeability of the alveolar-capillary membrane was studied, using horseradish peroxidase (HRP) as an ultrastructural marker. The alveolar-capillary membrane was impermeable to HRP at 4 weeks of corticosteroid treatment as well as in control rats. However, by 7 weeks, when the Type I pneumocyte started to show degenerative changes, HRP leaked through the capillary endothelium, indicating changes in the permeability of the alveolar-capillary membrane. We conclude that this increased permeability is the first change which triggers the subsequent degeneration of the Type I pneumocyte. The possible pathogenesis of this increased permeability of the alveolar-capillary membrane is discussed in relation to the organism's attachment to the alveolar epithelium.
mesh_terms: D000818:Animals; D002199:Capillary Permeability; D003348:Cortisone / Q000031:analogs & derivatives; D006735:Horseradish Peroxidase / Q000378:metabolism; D008297:Male; D008854:Microscopy, Electron; D011020:Pneumonia, Pneumocystis / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology*; D011650:Pulmonary Alveoli / Q000378:metabolism / Q000648:ultrastructure*; D051381:Rats; D011919:Rats, Inbred Strains
chemical_list: D006735:Horseradish Peroxidase; D003348:Cortisone