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1 Division of Pulmonary and Critical Care Medicine, Michael Reese Hospital, University of Illinois at Chicago, Chicago, Illinois 60616; and 2 Departamento de Enfermedades Respiratorias, Facultad de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile
Exposure of
adult rats to 100% O2 results in
lung injury and decreases active sodium transport and lung edema
clearance. It has been reported that 
-adrenergic agonists increase
lung edema clearance in normal rat lungs by upregulating alveolar
epithelial Na+-K+-ATPase
function. This study was designed to examine whether isoproterenol (Iso) affects lung edema clearance in rats exposed to 100%
O2 for 64 h. Active
Na+ transport and lung edema
clearance decreased by ~44% in rats exposed to acute hyperoxia. Iso
(10
6 M) increased the
ability of the lung to clear edema in room-air-breathing rats (from
0.50 ± 0.02 to 0.99 ± 0.05 ml/h) and in rats exposed to 100%
O2 (from 0.28 ± 0.03 to 0.86 ± 0.09 ml/h; P < 0.001). Disruption of intracellular microtubular transport
of ion-transporting proteins by colchicine (0.25 mg/100 g body wt)
inhibited the stimulatory effects of Iso in hyperoxia-injured rat
lungs, whereas the isomer -lumicolchicine, which does not affect
microtubular transport, did not inhibit active
Na+ transport stimulated by Iso.
Accordingly, Iso restored the lung's ability to clear edema after
hyperoxic lung injury, probably by stimulation of the recruitment of
ion-transporting proteins
(Na+-K+-ATPase)
from intracellular pools to the plasma membrane in rat alveolar epithelium.
active sodium transport; sodium-potassium-adenosinetriphosphatase; oxidant lung injury; -adrenergic
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