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1 Pulmonary and Critical Care Medicine, Northwestern University, Chicago 60611; 2 Evanston Northwestern Healthcare, Evanston, Illinois 60201; and 3 Pulmonary, Allergy and Critical Care, Departments of Medicine and Pediatrics, University of Minnesota, Minneapolis, Minnesota 55455
Acute hypoxemic respiratory failure is a consequence of edema accumulation due to elevation of pulmonary capillary pressures and/or increases in permeability of the alveolocapillary barrier. It has been recognized that lung edema clearance is distinct from edema accumulation and is largely effected by active Na+ transport out of the alveoli rather than reversal of the Starling forces, which control liquid flux from the pulmonary circulation into the alveolus. The alveolar epithelial Na+-K+-ATPase has an important role in regulating cell integrity and homeostasis. In the last 15 yr, Na+-K+-ATPase has been localized to the alveolar epithelium and its contribution to lung edema clearance has been appreciated. The importance of the alveolar epithelial Na+-K+-ATPase function is reflected in the changes in the lung's ability to clear edema when the Na+-K+-ATPase is inhibited or increased. An important focus of the ongoing research is the study of the mechanisms of Na+-K+-ATPase regulation in the alveolar epithelium during lung injury and how to accelerate lung edema clearance by modulating Na+-K+-ATPase activity.
acute respiratory distress syndrome; alveolar epithelium; ion transport
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