Previous studies have suggested that recovery from
pulmonary edema may be dependent on active
sodium ion transport. Most of the data supporting this concept came from work done in isolated type II cells, isolated lung preparations, or in models of alveolar flooding. There is a limited amount of information regarding the role of active
sodium ion transport in vivo. Furthermore, most of this information was obtained in one model of
pulmonary edema, the hyperoxic
lung injury model. The purpose of these experiments was then to measure the activity of the
sodium-potassium-adenosinetriphosphatase (Na(+)-K(+)-
ATPase), the active component of the
sodium transport process and an indirect marker of active
sodium transport, during recovery from
thiourea-induced
pulmonary edema in rats. Na(+)-K(+)-
ATPase activity was significantly increased during recovery from lung
edema. This increase could not be accounted for by the Na(+)-K(+)-
ATPase activity present in inflammatory cells recruited in the lung by the injury process or by a direct impact of
thiourea on the
enzyme. Alveolar flooding, induced by instillation of a
protein-containing
solution into the airways of ventilated rats also increased the activity of Na(+)-K(+)-
ATPase, suggesting that activation of the
enzyme is probably secondary to either the presence of
edema or the physiological consequences associated with
edema. The quantity of lung Na(+)-K(+)-
ATPase protein was also elevated during
edema resolution, indicating that augmented synthesis of this
enzyme underlies the increased
enzyme activity observed. The quantity of Na(+)-K(+)-
ATPase protein in alveolar type II cells was also significantly enhanced during recovery from
edema, suggesting that these cells contribute to active
sodium transport in vivo. The results of this study suggest that active
sodium transport could participate in the resolution of
pulmonary edema.