INCREASE OF LUNG SODIUM-POTASSIUM-ATPASE ACTIVITY DURING RECOVERY FROM HIGH-PERMEABILITY PULMONARY-EDEMA

Previous studies have suggested that recovery from pulmonary edema may be dependent on active sodium ion transport. Most of the data support ing this concept came from work done in isolated type II cells, isolat ed lung preparations, or in models of alveolar flooding. There is a li mited amount of information regarding the role of active sodium ion tr ansport in vivo. Furthermore, most of this information was obtained in one model of pulmonary edema, the hyperoxic lung injury model. The pu rpose of these experiments was then to measure the activity of the sod ium-potassium-adenosinetriphosphatase (Na+-K+-ATPase), the active comp onent of the sodium transport process and an indirect marker of active sodium transport, during recovery from thiourea-induced pulmonary ede ma 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 th e enzyme. Alveolar flooding, induced by instillation of a protein-cont aining solution into the airways of ventilated rats also increased the activity of Na+-K+-ATPase, suggesting that activation of the enzyme i s probably secondary to either the presence of edema or the physiologi cal consequences associated with edema. The quantity of lung Na+-K+-AT Pase protein was also elevated during edema resolution, indicating tha t augmented synthesis of this enzyme underlies the increased enzyme ac tivity observed. The quantity of Na+-K+-ATPase protein in alveolar typ e 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 c ould participate in the resolution of pulmonary edema.