Mechanisms of lung liquid clearance during hyperoxia in isolated rat lungs

J. I. Sznajder*, W. G. Olivera, K. M. Ridge, D. H. Rutschman

*Corresponding author for this work

Research output: Contribution to journalArticle

79 Scopus citations

Abstract

Sodium transport across the lung epithelium is predominantly effected by apical amiloride-sensitive Na+ channels and basolaterally located ouabain- sensitive Na,K-ATPases. Previously, we reported that subacute hyperoxia causes an increase in active Na+ transport in rat lungs paralleling Na,K- ATPase upregulation in alveolar Type 2 cells isolated from the same lungs. In the present study we set out to quantify the amiloride-sensitive Na+ flux and ouabain-sensitive active Na+ transport in the isolated-perfused, fluid- filled lung model from rats exposed to 85% O2 for 7 d compared with normoxic control rats. We found increased transpulmonary albumin flux and permeability to small solutes (Na+ and mannitol) in hyperoxic rat lungs compared with controls. Amiloride (10-5 M) instilled into rat airspaces inhibited active Na+ transport by ~62% in control rat lungs and by ~87% in lungs from rats exposed to hyperoxia, without further changing permeability for Na+ and mannitol. Ouabain (10-8 M) perfused through the pulmonary circulation decreased active Na+ transport by ~40% in normal rat lungs and by ~52% in lungs from rats exposed to hyperoxia. We conclude that active Na+ transport and edema clearance are increased in the subacute hyperoxic lung injury in rats, caused in part by the upregulation of amiloride-sensitive apical Na+ channels and alveolar epithelial Na,K-ATPases. Conceivably, the upregulation of alveolar epithelial Na+ channels and Na,K-ATPases protects against the effects of lung injury in this model by contributing to effective edema clearance.

Original languageEnglish (US)
Pages (from-to)1519-1525
Number of pages7
JournalAmerican journal of respiratory and critical care medicine
Volume151
Issue number5
DOIs
StatePublished - Jan 1 1995

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Critical Care and Intensive Care Medicine

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