Stress failure hypothesis

The alveolar fluid of high-altitude pulmonary edema patients has a high content of large proteins and contains numerous erythrocytes, suggesting a permeability leak in pulmonary capillaries. The stress failure hypothesis incorporates hydrostatic and permeability components. Hydrostatic stress applied to pulmonary vessels induces mechanical damage to pulmonary endothelial and epithelial cells. In addition, breaks in the capillary endothelial layer expose the basement membrane with activation of neutrophils and thrombocytes. Thrombin formation and the presence of inflammatory mediators (e.g. leukotriene B4 and complement fragment C5a) in the bronchoalveolar lavage fluid are possible consequences favoring both interstitial and alveolar edema.

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