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Enhancement of Alveolar Epithelial β2-Adrenergic Receptor Function Via Gene Transfer*

Phillip Factor, DO, FCCP; Zaher A. Azzam, MD; Gökhan M. Mutlu, MD; Jacob I. Sznajder, MD; Vidas Dumasius
Author and Funding Information

*From Pulmonary and Critical Care Medicine, Evanston Hospital, Evanston, IL; Northwestern University Medical School, Chicago, IL; and Technion, Israel Institute of Technology, Haifa, Israel.

Correspondence to: Phillip Factor, DO, FCCP, Pulmonary and Critical Care Medicine, Evanston Northwestern Healthcare, 2650 Ridge Rd, Evanston, IL 60201; e-mail: pfactor@northwestern.edu



Chest. 2002;121(3_suppl):45S-46S. doi:10.1378/chest.121.3_suppl.45S
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Extract

Pulmonary edema is removed from the airspace as a consequence of active Na+ transport by alveolar epithelial transport proteins, including basolaterally located Na,K-adenosine triphosphatases (ATPases) and apically positioned Na+ entry pathways such as the epithelial Na+ channel (ENaC). These transporters actively extrude Na+ from the airspace to generate a transepithelial osmotic gradient that causes movement of fluid from the airspace via transcellular and paracellular pathways. Accumulating data suggest that in some forms of acute lung injury active, Na+ transport is impaired, possibly due to downregulation of alveolar solute transport pathways.17 Thus, methods that improve alveolar Na+ transport could prove useful for the treatment of pulmonary edema.

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