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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.
K H Albertine
January 1988,
Nihon Kyobu Shikkan Gakkai zasshi,
K H Albertine
January 1981,
Annual review of medicine,
K H Albertine
June 1987,
The American journal of pathology,
K H Albertine
September 1981,
The American journal of medicine,
K H Albertine
September 1972,
The American review of respiratory disease,
K H Albertine
November 1988,
The American review of respiratory disease,
K H Albertine
September 1981,
Canadian Medical Association journal,
K H Albertine
December 1987,
The American review of respiratory disease,
