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Departments of Medicine, Physiology, Pathology and Nursing, Schools of Medicine and Pharmacy, University of Minnesota, Minneapolis, Minnesota 55455
Received 21 September 1995; accepted in final form 30 May 1996.
Lasnier, Joseph M., O. Douglas Wangensteen, Laura S. Schmitz, Cynthia R. Gross, and David H. Ingbar. Terbutaline
stimulates alveolar fluid resorption in hyperoxic lung injury.
J. Appl. Physiol. 81(4):
1723-1729, 1996.
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 from 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
(103 M), or both. Normoxic
animals resorbed 49 ± 6 µl · kg1 · min1;
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 · kg1 · min1;
ouabain reduced this by 44%. Terbutaline increased the rate by a mean
of 39 µl · kg1 · min1,
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.
ouabain; active sodium transport; sodium-potassium adenosinetriphosphatase; pulmonary edema
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