@article{3094147,
    title = "Hypocapnic but not metabolic alkalosis impairs alveolar fluid
reabsorption",
    author = "Myrianthefs, PM and Briva, A and Lecuona, E and Dumasius, V and and Rutschman, DH and Ridge, KM and Baltopoulos, GJ and Sznajder, JI",
    journal = "AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE",
    year = "2005",
    volume = "171",
    number = "11",
    pages = "1267-1271",
    publisher = "AMER THORACIC SOC",
    issn = "1073-449X",
    doi = "10.1164/rccm.200408-998OC",
    keywords = "alveolar epithelial cells; hypocapnic alkalosis; ion transport;
Na,K-ATPase; pulmonary edema",
    abstract = "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 (P-CO2; 10 and 20 mm Hg) independent
of pH levels (7.7 or 7.4). In addition, P-CO2 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 air-spaces. The effect of low P-CO2
on alveolar fluid reabsorption was reversible because clearance
normalized after correcting the P-CO2 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."
}