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1 Centre de Recherche du Centre Hospitalier de l'Université de Montréal and Département de Médecine, Université de Montréal, Montréal, Quebec, Canada H2W 1T7; 2 Department of Physiology, Northeastern Ohio Universities College of Medicine, Rootstown, Ohio 44272; and 3 Cardiovascular Research Institute and Department of Anesthesia and Medicine, University of California at San Francisco, San Francisco, California 94143
Resolution of pulmonary edema
involved active transepithelial sodium transport. Although several of
the cellular and molecular mechanisms involved are relatively well
understood, it is only recently that the regulation of these mechanisms
in injured lung are being evaluated. Interestingly, in mild-to-moderate
lung injury, alveolar edema fluid clearance is often preserved. This
preserved or enhanced alveolar fluid clearance is mediated by
catecholamine-dependent or -independent mechanisms. This stimulation of
alveolar liquid clearance is related to activation or increased
expression of sodium transport molecules such as the epithelial sodium
channel or the Na+-K+-ATPase pump and may also
involve the cystic fibrosis transmembrane conductance regulator. When
severe lung injury occurs, the decrease in alveolar liquid clearance
may be related to changes in alveolar permeability or to changes in
activity or expression of sodium or chloride transport molecules.
Multiple pharmacological tools such as 
-adrenergic agonists,
vasoactive drugs, or gene therapy may prove effective in stimulating
the resolution of alveolar edema in the injured lung.
lung injury; alveolar fluid clearance; sodium transport; -adrenergic agonists
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