Ultrastructural abnormalities in increased-permeability pulmonary edema.
A general clinical impression is that increased microvascular permeability following acute lung injury always leads to pulmonary edema. The ARDS is a final pathway of acute lung injury. A number of agents may initiate acute lung injury, either directly or indirectly, via cellular and humoral mediators. Clinical and experimental animal studies indicate that both the microvascular and alveolar-airway barriers are susceptible to injury. Unfortunately, the spectrum of cellular damage is nonspecific and quite uniform, regardless of the injurious agent. Thus pathologic examination often reveals little about the exact underlying etiology of the lung injury. This situation has minimized the diagnostic value of lung biopsies in clinical cases of increased-permeability pulmonary edema. Nonetheless, the pathologic information has been, and will continue to be, invaluable to understanding the structural and functional relationships present in experimental models of increased-permeability pulmonary edema.
D000531:Altitude; D000818:Animals; D001798:Blood Proteins / Q000378:metabolism; D002199:Capillary Permeability; D005374:Filtration; D006801:Humans; D008168:Lung / Q000648:ultrastructure*; D008833:Microcirculation; D011652:Pulmonary Circulation; D011654:Pulmonary Edema / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology
D001798:Blood Proteins