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Service de Chirurgie Thoracique et Cardiovasculaire, Centre Hospitalier Universitaire de Caen, 14000 Caen; and Institut National de la Santé et de la Recherche Médicale Unité 82, Faculté Xavier Bichat, 75018 Paris, France
We have
developed a simple isolated lung preparation for measurement of liquid
and solute fluxes across mouse alveolar epithelium. Liquid instilled
into air spaces was absorbed at the rate
(Jw) of 3.7 ± 0.32 ml · h
1 · g
dry lung wt1.
Jw was
significantly depressed by ouabain (P < 0.001) and amiloride (P < 0.001). Omission of glucose from the instillate or addition of the
Na+-glucose cotransport inhibitor
phloridzin did not affect
Jw. However, the
low epithelial lining fluid glucose concentration (one-third that of
plasma), the larger-than-mannitol permeability of
methyl-
-D-glucopyranoside, and the presence of Na+-glucose
cotransporter SGLT1 mRNA in mouse lung tissue suggest that there is a
Na+-glucose cotransporter in the
mouse alveolar-airway barrier. Isoproterenol stimulated
Jw (6.5 ± 0.45 ml · h1 · g
dry lung wt1;
P < 0.001), and this effect was
blocked by amiloride, benzamil, ouabain, and the specific
2-adrenergic antagonist
ICI-118551 but not by atenolol. Similar stimulation was obtained with
terbutaline (6.4 ± 0.46 ml · h1 · g
dry lung wt1).
Na+ unidirectional fluxes out of
air spaces varied in agreement with Jw changes. Thus
alveolar liquid absorption in mice follows
Na+ transport via the
amiloride-sensitive pathway, with little contribution from
Na+-glucose cotransport, and is
stimulated by 2-adrenergic agonists.
glucose transport; pulmonary alveoli; pulmonary edema
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