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1 Atlanta Veterans Affairs Medical Center, Decatur 30033; Departments of 2 Medicine and 4 Pediatrics, Emory University, Atlanta, Georgia 30322; and 3 Department of Anesthesiology, University of California, San Francisco, California 94143
We determined that rats fed a liquid
diet containing ethanol (36% of calories) for 6 wk had decreased
(P < 0.05) net vectorial fluid transport and increased
(P < 0.05) bidirectional protein permeability across
the alveolar epithelium in vivo compared with rats fed a control diet.
However, both groups increased (P < 0.05) fluid
transport in response to epinephrine (10
5 M) stimulation,
indicating that transcellular sodium transport was intact. In parallel,
type II cells isolated from ethanol-fed rats and cultured for 8 days
formed a more permeable monolayer as reflected by increased
(P < 0.05) leak of [14C]inulin. However,
type II cells from ethanol-fed rats had more sodium-permeant channels
in their apical membranes than type II cells isolated from control-fed
rats, consistent with the preserved response to epinephrine in vivo.
Finally, the alveolar epithelium of ethanol-fed rats supplemented with
L-2-oxothiaxolidine-4-carboxylate (Procysteine), a
glutathione precursor, had the same (P < 0.05) net
vectorial fluid transport and bidirectional protein permeability in
vivo and permeability to [14C]inulin in vitro as
control-fed rats. We conclude that chronic ethanol ingestion via
glutathione deficiency increases alveolar epithelial intercellular
permeability and, despite preserved or even enhanced transcellular
sodium transport, renders the alveolar epithelium susceptible to acute
edematous injury.
alcoholism; acute respiratory distress syndrome; endotoxin; lung
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