Abstract
Clearance of pulmonary edema fluid is accomplished by active ion transport, predominantly by the alveolar epithelium. Various ion pumps and channels on the surface of the alveolar epithelial cell generate an osmotic gradient across the epithelium, which in turn drives the movement of water out of the airspaces. Here, the mechanisms of alveolar ion and fluid clearance are reviewed. In addition, many factors that regulate the rate of edema clearance, such as catecholamines, steroids, cytokines, and growth factors, are discussed. Finally, we address the changes to the alveolar epithelium and its transport processes during acute lung injury (ALI). Since relevant clinical outcomes correlate with rates of edema clearance in ALI, therapies based on our understanding of the mechanisms and regulation of fluid transport may be developed.
Highlights
In the normal lung, fluid moves from the blood circulation through the capillary endothelium into the lung interstitium and is cleared by the lymphatics on a continuous basis
Regulation of alveolar fluid transport in acute lung injury β-Agonists In a model of septic shock in rats, endogenous plasma adrenaline levels are 100 times higher than normal, and this increase is associated with a 100% increase in alveolar fluid clearance (AFC) – an effect that is prevented with β-blockers
Our understanding of the mechanisms of AFC in normal states and acute lung injury (ALI) will lead to better treatment modalities for ALI, a diagnosis that carries significant morbidity and mortality
Summary
Fluid moves from the blood circulation through the capillary endothelium into the lung interstitium and is cleared by the lymphatics on a continuous basis. There are some endogenous mechanisms by which this may occur, but we AFC = alveolar fluid clearance; ALI = acute lung injury; AQP = aquaporin; ENaC = epithelial Na+ channel; HGF = hepatocyte growth factor; IL = Fluid clearance from the airspaces in the setting of pulmonary edema depends on sodium transport through channels that are located on the apical surfaces of alveolar epithelial cells.
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