Journal
CLINICS IN CHEST MEDICINE
Volume 21, Issue 3, Pages 435-+Publisher
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1016/S0272-5231(05)70158-1
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The pulmonary pathologic features of acute respiratory distress syndrome (ARDS) reflect a dynamic, rapidly progressive transition from acute alveolocapillary injury through edema and cellular exudation to diffuse alveolar fibroplasia and end-stage collagenization-a process termed diffuse alveolar damage. Intraluminal organization and fibrosis within alveoli and alveolar ducts are key mechanisms of fibrous remodeling. The pulmonary vasculature also is affected severely by a variety of thrombotic, fibroproliferative and obliterative changes, which result in pulmonary hypertension. Individual pulmonary lesions are nonspecific and consistent with the complex interaction of numerous injurious agents and inflammatory mediators acting on alveolar epithelial and endothelial cells. At the molecular level, factors that influence apoptosis and cellular proliferation may be important in the evolution of progressive lung modeling.
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