Journal of Applied Physiology
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J Appl Physiol 87: 962-968, 1999;
8750-7587/99 $5.00
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Vol. 87, Issue 3, 962-968, September 1999

Impairment of transalveolar fluid transport and lung Na+-K+-ATPase function by hypoxia in rats

Satoshi Suzuki1, Masafumi Noda1, Makoto Sugita1, Sadafumi Ono1, Kaoru Koike2, and Shigefumi Fujimura1

1 Department of Thoracic Surgery, Institute of Development, Aging, and Cancer, Tohoku University, Aoba-ku, Sendai 980-8575; and 2 Department of Thoracic Surgery, Miyagi Cancer Center, Medeshima-Shiode, Natori 981-1293, Japan

We examined whether hypoxic exposure in vivo would influence transalveolar fluid transport in rats. We found a significant decrease in alveolar fluid clearance of the rats exposed to 10% oxygen for 48 h. Terbutaline did not stimulate alveolar fluid clearance, and alveolar fluid cAMP levels were lower than those determined in normoxia experiment. Hypoxia did not influence the alveolar fluid lactate dehydrogenase levels, Evans blue dye fluid-to-serum concentration ratio, or lung wet-to-dry weight ratio, indicating no significant change in the permeability of alveolar-capillary barrier. Histological examination showed no significant fluid accumulation into the interstitium and the alveolar space. Hypoxia did not reduce lung ATP content; however, we found significant decrease in Na+-K+-ATPase hydrolytic activity in lung tissue preparations and isolated alveolar type II cells. Our data indicate that hypoxic exposure in vivo impairs transalveolar fluid transport, and this impairment is related to the decrease in alveolar epithelial Na+-K+-ATPase hydrolytic activity but is not secondary to the alteration of cellular energy source.

hypoxia; alveolar fluid clearance; alveolar type II cells; beta -adrenergic agonists


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