title: Hyperoxic effects on alveolar sodium resorption and lung Na-K-ATPase.
abstract: 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 x surface area products for unidirectional resorption of alveolar [14C]sucrose (PSsucrose) and 22Na+ (PSNa+) 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 PSsucrose and PSNa+ increased from 6.71 +/- 0.8 x 10(-5) to 12.6 +/- 1.6 x 10(-5) cm3/s (P = 0.029) and from 23.6 +/- 1.1 x 10(-5) to 31.0 +/- 1.6 x 10(-5) cm3/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) PSNa+ was significantly reduced in the exposed lungs with normal PSsucrose but was maintained in the lungs with high PSsucrose. By day 3 of recovery, mean Na+ and sucrose fluxes returned to values similar to control. Na-K-ATPase membrane hydrolytic maximal velocity (Vmax) activity fell significantly immediately after hyperoxic exposure but recovered to normal values by day 3 of recovery. The Na-K-ATPase beta 1-subunit antigenic signal did not significantly change, whereas the alpha 1-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.
authors.affiliation: Department of Physiology, School of Medicine, University of Minnesota, Minneapolis 55455, USA.
authors.forename: E P
authors.initials: EP
authors.lastname: Carter
authors.forename: O D
authors.initials: OD
authors.lastname: Wangensteen
authors.forename: J
authors.initials: J
authors.lastname: Dunitz
authors.forename: D H
authors.initials: DH
authors.lastname: Ingbar
mesh_terms: D000584:Amiloride / Q000031:analogs & derivatives / Q000494:pharmacology; D000818:Animals; D002462:Cell Membrane / Q000201:enzymology; D004847:Epithelial Cells / Q000502:physiology; D018496:Hyperoxia; D066298:In Vitro Techniques; D007700:Kinetics; D008168:Lung / Q000201:enzymology* / Q000503:physiopathology; D008297:Male; D010539:Permeability; D011650:Pulmonary Alveoli / Q000502:physiology* / Q000503:physiopathology; D011651:Pulmonary Artery / Q000187:drug effects / Q000502:physiology* / Q000503:physiopathology; D011654:Pulmonary Edema; D051381:Rats; D017207:Rats, Sprague-Dawley; D012964:Sodium / Q000378:metabolism*; D015222:Sodium Channels / Q000502:physiology; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*; D013499:Surface Properties
chemical_list: D015222:Sodium Channels; C013407:benzamil; D000584:Amiloride; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase