Mechanism of pulmonary alveolar injury in experimental Pneumocystis carinii pneumonia in the rat.
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.
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
D006735:Horseradish Peroxidase; D003348:Cortisone