Increase of lung sodium-potassium-atpase activity during recovery
from high-permeability pulmonary edema.
Zuege, Danny, Satoshi Suzuki, and Yves Berthiaume.
Centre de Recherche H[circumflex]otel-Dieu de Montr[acute]eal and
Department of Medicine, Universit[acute]e de Montr[acute]eal,
Montreal, Quebec, Canada
APStracts 3:0137L, 1996.
Previous studies have suggested that recovery from pulmonary edema may
be dependent on active sodium ion transport. Most of the data
supporting this concept came from work done in isolated type II
cells, isolated lung preparations or in models of alveolar flooding.
There is a limited amount of information regarding the role of active
Na+ transport in vivo. Furthermore, most of this information was
obtained in one model of pulmonary edema, the hyperoxic lung injury
model. The purpose of these experiments was then to measure the
activity of the sodium-potassium adenosine triphosphatase (Na+-K+
-ATPase), the active component of the sodium transport process and an
indirect marker of active sodium transport, during recovery from
thiourea-induced pulmonary edema in rats. Na+-K+-ATPase activity was
significantly increased during recovery from lung edema. This
increase could not be accounted for by the Na+-K+-ATPase activity
present in inflammatory cells recruited in the lung by the injury
process or by a direct impact of thiourea on the enzyme. Alveolar
flooding, induced by instillation of a protein-containing solution
into the airways of ventilated rats, also increased the activity of
Na+-K+-ATPase, suggesting that activation of the enzyme is probably
secondary to either the presence of edema or the physiologic
consequences associated with edema. The quantity of lung Na+-K+
-ATPase protein was also elevated during edema resolution, indicating
that augmented synthesis of this enzyme underlies the increased
enzyme activity observed. The quantity of Na+-K+-ATPase protein in
alveolar type II cells was also significantly enhanced during
recovery from edema, suggesting that these cells contribute to active
sodium transport in vivo. The results of this study suggest that
active sodium transport could participate in the resolution of
pulmonary edema.
Received 23 January 1995; accepted in final form 15 July 1996.
APS Manuscript Number L19-5.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 29 August 1996