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Department of Animal Physiology, Lund University, S-223 62 Lund, Sweden
Alveolar liquid clearance was examined in
ventilated, anesthetized guinea pigs. An isosmolar 5% albumin solution
was instilled into the lungs. Alveolar liquid clearance was studied
over 1 h and was measured from the increase in alveolar protein
concentration as water was reabsorbed. Basal alveolar liquid clearance
was 38% of instilled volume. The high basal alveolar liquid clearance was not secondary to endogenous catecholamine release. Compared with
control animals, epinephrine and the general
-adrenergic agonist
isoproterenol increased alveolar liquid clearance to ~50% of
instilled volume (P < 0.05), whereas
the
2-adrenergic agonist terbutaline was without effect. The stimulation of alveolar liquid clearance by epinephrine or isoproterenol was completely inhibited by
the addition of the general
-adrenergic inhibitor propranolol or the
1-adrenergic inhibitor
atenolol. Alveolar liquid clearance was inhibited by the sodium-channel
inhibitor amiloride by 30-40% in control animals and in animals
treated with epinephrine or isoproterenol. Isoproterenol and
epinephrine, but not terbutaline, increased adenosine
3',5'-cyclic monophosphate in in vitro incubated lung
tissue. The results suggest that alveolar liquid clearance in guinea
pigs is mediated partly through amiloride-sensitive sodium channels and
that alveolar liquid clearance can be increased by stimulation of
primarily
1-adrenergic
receptors.
amiloride;
-adrenergic stimulation; adenosine
3',5'-cyclic monophosphate generation; epinephrine; lung
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