Alveolar fluid resorption occurs by active epithelial sodium transport and is accelerated by terbutaline in healthy lungs. We investigated the effect of terbutaline on the rate of alveolar fluid resorption froth rat lungs injured by hyperoxia. Rats exposed to >95% O2 for 60 h, sufficient to increase wet-to-dry lung weight and cause alveolar edema, were compared with air-breathing control rats. After anesthesia, the animals breathed 100% O2 for 10 min through a tracheostomy. Ringer solution was instilled into the alveoli, and the steady-state rate of volume resorbed at 6 cmH2O pressure was measured via a pipette attached to the tracheostomy tubing. Ringer solution in some animals contained terbutaline (10-3 M), ouabain (10-3 M), or both. Normoxic animals resorbed 49 ± 6 μl · kg-1 · min-1; ouabain reduced this by 39%, whereas terbutaline increased the rate by 75%. The effect of terbutaline was blocked by ouabain. Hyperoxic animals absorbed 78 ± 9 μl · kg-1 · min-1; ouabain reduced this by 44%. Terbutaline increased the rate by a mean of 39 μl · kg-1 · min-1, similar to the absolute effect seen in the normoxic group, and this was blocked by ouabain. Terbutaline accelerates fluid resorption from both normal and injured rat lungs via its effects on active sodium transport.
- active sodium transport
- pulmonary edema
- sodium-potassium adenosinetriphosphatase