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Department of Physiology and Pharmacology, School of Medicine, University of South Dakota, Vermillion, South Dakota 57069
Received 19 January 1995; accepted in final form 28 August 1996.
Zheng, Lu P., Rui Sheng Du, and Barbara E. Goodman.
Effects of acute hyperoxic exposure on solute fluxes across the blood-gas barrier in rat lungs. J. Appl.
Physiol. 82(1): 240-247, 1997.
We investigated
effects of acute hyperoxia on solute transport from air space to
vascular space in isolated rat lungs. Air spaces were filled with
Krebs-Ringer bicarbonate solution containing fluorescein
isothiocyanate-labeled dextran (FD-20; mol wt 20,000) and either
22Na+
and [14C]sucrose, or
D-[14C]glucose
and
L-[3H]glucose.
Apparent permeability-surface area products for tracers over time (up
to 120 min) were calculated for isolated perfused lungs from control
rats (room air) and rats exposed to >95%
O2 for 48 or 60 h immediately
postexposure. After O2 exposures,
mean fluxes for
[14C]sucrose and FD-20
were significantly higher than in room-air control lungs. However,
amiloride-sensitive Na+ 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 O2 toxicity.
Increased net solute transport shown to help resolve pulmonary edema
after 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 after acute
hyperoxic lung injury.
amiloride; phloridzin; oxygen toxicity; pulmonary edema
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