Impairment of transalveolar fluid transport and lung na-/k--atpase function by hypoxia in rats. Suzuki, Satoshi, Masafumi Noda, Makoto Sugita, Sadafumi Ono, Kaoru Koike and Shigefumi Fujimura. 1Department of Thoracic Surgery, Institute of Development, Aging and Cancer, Tohoku University, 4-1 Seiryo-machi, Aoba-ku, Sendai, JAPAN 980-8575 and 2Department of Thoracic Surgery, Miyagi Cancer Center, 47-1 Nodaya, Medeshima-Shiode, Natori, JAPAN, 981-1293
APStracts 6:0239A, 1999.
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 hours. 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 (LDH) levels, Evans blue dye fluid/serum concentration ratio or lung wet/dry weight ratio, indicating no significant change 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 not secondary to the alteration of cellular energy source.

Received 30 October 1998; accepted in final form 26 May 1999.
APS Manuscript Number A1087-8.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1999 The American Physiological Society.
Published in APStracts on 14 June 1999