Effects of acute hyperoxic exposure on solute fluxes across the
blood-gas barrier in rat lungs.
Zheng, Lu P., Rui Sheng Du, Barbara E. Goodman.
Department of Physiology and Pharmacology, School of Medicine,
University of South Dakota, Vermillion, SD 57069
APStracts 3:0428A, 1996.
We investigated effects of acute hyperoxia on solute transport from
airspace to vascular space in isolated rat lungs. Airspaces were
filled with Krebs-Ringer bicarbonate solution containing FITC
-labelled dextran (FD20, M.W. 20,000) and either 22Na and 14C-sucrose,
or 14C-D-glucose and 3H-L-glucose. Apparent permeability-surface area
products (PS) for tracers over time (up to 120 min) were calculated
for isolated perfused lungs from room air-control rats and rats
exposed to >95% oxygen for 48 h or 60 h immediately
postexposure. After oxygen exposures, mean fluxes for 14C-sucrose and
FD20 were significantly higher than room air-control lungs. However,
amiloride-sensitive sodium and active D-glucose fluxes were unchanged
after hyperoxic exposure. Therefore, it is unlikely that decreases in
net solute transport in this lung injury model contributed to
pulmonary edema resulting from oxygen toxicity. Increased net solute
transport shown to help resolve pulmonary edema following acute
hyperoxic exposure must therefore begin during the recovery period.
In summary, our data show increases in passive solute fluxes but no
changes in active solute fluxes immediately following acute hyperoxic
lung injury.
Received 19 January 1995; accepted in final form 28 August 1996.
APS Manuscript Number A69-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 7 October 1996