Abstract
Acute respiratory distress syndrome (ARDS) is characterized by hypoxemia from flooding of the distal airspaces of the lung with protein-rich edema fluid. Pulmonary edema develops because of an increase in lung vascular permeability and from injury to the alveolar epithelium that diminishes the normal capacity of the alveolar epithelium to remove edema fluid from the airspaces (alveolar fluid clearance, AFC) (1, 2). The severity of alveolar edema depends on the competing effects of increased permeability and the active clearance of edema fluid from the airspaces in regions where the epithelium is intact. The vectorial transport of sodium into the interstitial space provides an osmotic gradient for absorption of water. The sodium concentration gradient is established by Na+/K+-ATPase located in the basolateral membrane of polarized alveolar epithelial type 1 and type 2 cells (Fig. 1). Transepithelial sodium transport also requires an adequate paracellular barrier, apically polarized sodium channels such as ENaC (the epithelial sodium channel), and chloride transport (3, 4).
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