Isoproterenol improves ability of lung to clear edema in rats exposed to hyperoxia

Exposure of adult rats to 100% O-2 results in lung injury and decreases act ive sodium transport and lung edema clearance. It has been reported that be ta-adrenergic agonists increase lung edema clearance in normal rat lungs by upregulating alveolar epithelial Na+-K+-ATPase function. This study was de signed to examine whether isoproterenol (Iso) affects lung edema clearance in rats exposed to 100% O-2 for 64 h. Active Na+ transport and lung edema c learance decreased by similar to 44% in rats exposed to acute hyperoxia. Is o (10(-6) M) increased the ability of the lung to clear edema in room-air-b reathing rats (from 0.50 +/- 0.02 to 0.99 +/- 0.05 ml/h) and in rats expose d to 100% O-2 (from 0.28 +/- 0.03 to 0.86 +/- 0.09 ml/h; P < 0.001). Disrup tion of intracellular microtubular transport of ion-transporting proteins b y colchicine (0.25 mg/100 g body wt) inhibited the stimulatory effects of I so in hyperoxia-injured rat lungs, whereas the isomer beta-lumicolchicine, which does not affect microtubular transport, did not inhibit active Na+ tr ansport stimulated by Iso. Accordingly, Iso restored the lung's ability to clear edema after hyperoxic lung injury, probably by stimulation of the rec ruitment of ion-transporting proteins (Na+-K+-ATPase) from intracellular po ols to the plasma membrane in rat alveolar epithelium.