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Hypoxia 2009 Speakers
Sadis Matalon
Alice McNeal Professor of Anesthesiology, University of Alabama at Birmingham
Email: sadis@uab.edu;tpotter@uab.edu
Talk Title: Mechanisms of impaired alveolar ion transport
Session: Lung fluid movement in hypoxia
Abstract: The mammalian alveolar epithelium transports Na+ ions from the alveolar lumen into the interstitial space. Na+ ions enter the apical membrane of alveolar epithelial type II (ATII) cells mainly through amiloride-sensitive Na+ channels and are actively transported across their basolateral membranes by the ouabain-sensitive Na,K-ATPase. This active Na+ transport subsequently drives fluid passively out of the alveolar space, and plays an important role in decreasing lung water in patients with acute respiratory distress syndrome (ARDS). Significantly, substances that block the entry of Na+ ions into ATII cells also increase lung water in animals with ARDS-type injury. Because of their location, alveolar epithelial cells are exposed continuously to various endogenous and exogenous oxidants, including nitric oxide (•NO). In addition, exposure of animal and human alveolar macrophages and epithelial cells to inflammatory mediators leads to an upregulation of the inducible form of nitric oxide synthase and elevated •NO over long periods of time. Because •NO is a free radical, it can undergo a radical-radical reaction with superoxide (O2•-) to yield peroxynitrite (ONOO-), a potent oxidizing and nitrating species. Existing evidence in the literature and our own data indicate that •NO and ONOO- modify the activity of ion channels either by altering signal transduction pathways or interacting with channel proteins directly. •NO and ONOO-, at non-cytotoxic concentrations, decreased Na+ absorption across cultured ATII monolayers by inhibiting both the amiloride-sensitive Na+ channels and the Na,K-ATPase, through cGMP-independent mechanisms. This observation has important implications in the clearance of alveolar fluid in patients with acute respiratory distress syndrome.

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