Hyperoxic effects on alveolar sodium resorption and lung Na-K-ATPase.

Active Na+ transport by the alveolar epithelium keeps alveoli relatively dry. Hyperoxia increases epithelial permeability, resulting in pulmonary edema. We sought to determine whether active Na+ resorption from the air spaces and Na-K-ATPase activity increased in rats exposed to >95% O2 for 60 h. The permeability × surface area products for unidirectional resorption of alveolar [14C]sucrose ( PS sucrose) and22Na+([Formula: see text]) were measured in isolated, perfused rat lungs immediately after hyperoxia and after 3 and 7 days of recovery in room air. At 60 h of hyperoxia, the mean PS sucrose and[Formula: see text]increased from 6.71 ± 0.8 × 10-5 to 12.6 ± 1.6 × 10-5cm3/s ( P = 0.029) and from 23.6 ± 1.1 × 10-5 to 31.0 ± 1.6 × 10-5cm3/s ( P < 0.008), respectively. However, the values in individual rats ranged widely from no change to nearly a fourfold increase. Subgroup analysis revealed that benzamil- or amiloride-sensitive (transcellular)[Formula: see text]was significantly reduced in the exposed lungs with normal PS sucrose but was maintained in the lungs with high PS sucrose. By day 3of recovery, mean Na+ and sucrose fluxes returned to values similar to control. Na-K-ATPase membrane hydrolytic maximal velocity ( V max) activity fell significantly immediately after hyperoxic exposure but recovered to normal values by day 3 of recovery. The Na-K-ATPase β1-subunit antigenic signal did not significantly change, whereas the α1-subunit levels increased during recovery. In summary, there was a heterogeneous response of different rats to acute hyperoxia. Hyperoxia led to complex, nonparallel changes in Na+ pump antigenic protein, hydrolytic activity, and unidirectional active Na+ resorption. Active Na+ transport was differentially affected, depending on degree of injury, but permeability and transport normalized by day 3 of recovery.