Exposure of rats to hyperoxia is associated with increased active Na+ transport in rat lungs and increased Na,K-adenosine triphosphate (ATPase) expression in alveolar epithelial cells. Hyperbaric oxygenation (HBO) has been reported to act as an accelerated model of hyperoxic cell damage. Sublethal and intermittent exposure to HBO, however, has been suggested to upregulate endogenous protective mechanisms. In the present study, we tested whether short-term HBO, prior to inducing lung injury, would upregulate lung Na,K-ATPase. The results show that HBO, either intermittent or single 2.5 h exposure, increased lung Na,K-ATPase α-1 and β-1 messenger ribonucleic acid (mRNA) transcript levels up to fourfold. Na,K-ATPase activity in lungs of rats exposed to HBO increased twofold during the first 2 h following removal from the hyperbaric chamber, and remained elevated for up to 6 h following HBO. Conceivably, the increase in Na,K-ATPase activity following HBO is due to an increase in activity from a basal to a higher rate, or possibly due to recruitment/translocation of Na,K-ATPases from inner membranes to the plasma membrane.
- alveolar Na,K-ATPase
- hyperbaric oxygenation
- lung injury
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine