ACTIVE SODIUM-TRANSPORT AND ALVEOLAR EPITHELIAL NA-K-ATPASE INCREASE DURING SUBACUTE HYPEROXIA IN RATS

Active Na+ transport and lung edema clearance were studied in a model of lung injury caused by sublethal oxygen exposure. Rats exposed to 85 % O-2 for 7 days were studied at 0, 7, 14, and 30 days after removal f rom the hyperoxic chamber and compared with room air controls. In the isolated-perfused, fluid-filled rat lung, albumin flux from the perfus ate into the air spaces increased after oxygen exposure and returned t o control values after 7 days of recovery. However, permeability to sm all solutes (Na+ and mannitol) normalized only after 30 days of recove ry from hyperoxia. Active Na+ transport increased immediately after ox ygen exposure and returned to control values 7 days after removal from hyperoxic chamber. Na-K-adenosinetriphosphatase (ATPase) activity, an d protein expression in alveolar epithelial type II cells obtained at the end of the isolated lung experiments increased significantly after the oxygen exposure compared with controls in association with the in creased active Na+ transport. We conclude that active Na+ transport an d lung liquid clearance are increased in the subacute hyperoxic phase of lung injury in rats, due in part to the upregulation of alveolar ep ithelial Na-K-ATPases. Conceivably, this behavior protects against the effects of lung injury by allowing the injured lung to clear edema mo re effectively. Accordingly, this upregulation may be targeted as a st rategy to diminish edema in patients with lung injury.