Salt and water transport across alveolar and distal airway
epithelia in the adult lung.
Matthay, Michael A., Hans G. Folkesson, and A. S. Verkman.
CARDIOVASCULAR RESEARCH INSTITUTE AND Departments of Medicine,
Anesthesia, and Physiology, University of California, San
Francisco
APStracts 3:0017L, 1996.
Substantial progress has been made in understanding the role of the
distal airway and alveolar epithelial barriers in regulating lung
fluid balance. Molecular, cellular, and whole animal studies have
demonstrated that reabsorption of fluid from the distal air spaces of
the lung is driven by active sodium transport. Several different in
vivo, in situ, and isolated lung preparations have been used to study
the mechanisms that regulate fluid transport in the normal and
injured lung. Catecholamine dependent and independent regulatory
mechanisms have been identified which modulate fluid transport,
probably by acting on apical sodium channel uptake or the activity of
the Na,K-ATPase pumps. Recently, a family of molecular water channels
(aquaporins) has been identified which are small (30 kDa) integral
membrane proteins expressed widely in fluid-transporting epithelia
and endothelia. At present, 4 different water channels have been
identified in trachea and lung. Measurements of osmotic water
permeability in in situ perfused lung and isolated perfused airways
suggest a significant contribution of these molecular water channels
to measured water permeability. However, further studies are required
to determine the role of these water channels in normal pulmonary
physiology and disease. Recent studies have provided new insights
into the role of the alveolar epithelial barrier in clinical and
experimental acute lung injury. Unlike the lung endothelium, the
alveolar epithelium is resistant to several clinically relevant types
of injury including endotoxemia and bacteremia as well as aspiration
of hyperosmolar solutions. In addition, even when the alveolar
barrier has been injured, its capacity to transport edema fluid from
the distal air spaces of the lung recovers rapidly. Future studies
need to integrate new insights into the molecular mechanisms of
alveolar epithelial sodium and water transport with functional
studies in the the normal and injured lung.
Received 18 September 1995; accepted in final form 16 January
1996.
APS Manuscript Number L277-5.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 29 January 96