Journal of Applied Physiology, Vol 60, Issue 5 1797-1809, Copyright © 1986 by American Physiological Society
Effect of 100% O2 on passage of uncharged dextrans from blood to lung lymph
J. H. Hansen-Flaschen, P. N. Lanken, G. G. Pietra, P. M. Sampson, L. Johns and A. P. Fishman
Since charge as well as size may influence the passage of plasma proteins
from blood to lung lymph, we used uncharged dextrans as tracers to study
the effects of hyperoxic lung injury on the molecular sieving properties of
the pulmonary microcirculation in unanesthetized sheep. Polydisperse
[3H]dextran was infused intravenously into five sheep before and after the
animals breathed 100% O2 until lymph flow increased threefold (66-84 h).
Lymph-to-plasma concentration ratios (L/P) were determined for [3H]dextran
fractions of graded molecular sizes (1.6-8.4 nm effective radius) from
samples obtained during the infusions. Before hyperoxia the blood-lymph
barrier was highly restrictive to transport of [3H]dextrans above 5.0 nm in
radius; steady-state L/P for these molecules averaged 0.03 or less. After
the sheep breathed 100% O2, [3H]dextrans as large as 8.4 nm radius appeared
in the lymph. Posthyperoxia, the L/P were significantly increased relative
to prehyperoxia base-line values for every [3H]dextran fraction larger than
2.0 nm radius (P less than 0.05). In contrast, neither the L/P for albumin
or total protein changed significantly. At autopsy, electron microscopy
showed widespread damage to the endothelium of the alveolar capillaries
with infrequent gaps between endothelial cells. In two control sheep,
inhalation of compressed air for 96 h had no effect on lymph flow or L/P
for the [3H]dextrans. We conclude that O2 poisoning reduced the selective
sieving of uncharged dextrans across the blood-lymph barrier of the lungs
and allowed larger dextrans to enter the lymph. These larger molecules may
have leaked from the pulmonary microcirculation via disruptions in the
continuity of the endothelial lining.
