Published ahead of print on March 11, 2005, doi:10.1164/rccm.200408-998OC
© 2005 American Thoracic Society doi: 10.1164/rccm.200408-998OC
Hypocapnic but Not Metabolic Alkalosis Impairs Alveolar Fluid ReabsorptionDivision of Pulmonary and Critical Care Medicine, Northwestern University; Medical Service, Veterans Affairs, Chicago Health Care System; Department of Mathematics, Northeastern Illinois University, Chicago, Illinois; Intensive Care Unit, "KAT" General Hospital, Athens University, Athens, Greece; and Departamento de Fisiopatologia, Facultad de Medicina, Universidad de la Republica, Montevideo, Uruguay Correspondence and requests for reprints should be addressed to Jacob I. Sznajder, M.D., Division of Pulmonary and Critical Care Medicine, 240 East Huron, McGaw 2-2300, Northwestern University, Feinberg School of Medicine, Chicago, IL 60611. E-mail: j-sznajder{at}northwestern.edu Acid-base disturbances, such as metabolic or respiratory alkalosis, are relatively common in critically ill patients. We examined the effects of alkalosis (hypocapnic or metabolic alkalosis) on alveolar fluid reabsorption in the isolated and continuously perfused rat lung model. We found that alveolar fluid reabsorption after 1 hour was impaired by low levels of CO2 partial pressure (PCO2; 10 and 20 mm Hg) independent of pH levels (7.7 or 7.4). In addition, PCO2 higher than 30 mm Hg or metabolic alkalosis did not have an effect on this process. The hypocapnia-mediated decrease of alveolar fluid reabsorption was associated with decreased Na,K-ATPase activity and protein abundance at the basolateral membranes of distal airspaces. The effect of low PCO2 on alveolar fluid reabsorption was reversible because clearance normalized after correcting the PCO2 back to normal levels. These data suggest that hypocapnic but not metabolic alkalosis impairs alveolar fluid reabsorption. Conceivably, correction of hypocapnic alkalosis in critically ill patients may contribute to the normalization of lung ability to clear edema.
Key Words: alveolar epithelial cells hypocapnic alkalosis ion transport Na,K-ATPase pulmonary edema This article has been cited by other articles:
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