Invited Review: Alveolar edema fluid clearance in the injured lung

Author:

Berthiaume Yves1,Folkesson Hans G.2,Matthay Michael A.3

Affiliation:

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

Abstract

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 β-adrenergic agonists, vasoactive drugs, or gene therapy may prove effective in stimulating the resolution of alveolar edema in the injured lung.

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology

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