A. Norlin et al., ALVEOLAR LIQUID CLEARANCE IN THE ANESTHETIZED VENTILATED GUINEA-PIG, American journal of physiology. Lung cellular and molecular physiology, 18(2), 1998, pp. 235-243
Alveolar liquid clearance was examined in ventilated, anesthetized gui
nea pigs. An isosmolar 5% albumin solution was instilled into the lung
s. Alveolar liquid clearance was studied over 1 h and was measured fro
m the increase in alveolar protein concentration as water was reabsorb
ed. Basal alveolar liquid clearance was 38% of instilled volume. The h
igh basal alveolar liquid clearance was not secondary to endogenous ca
techolamine release. Compared with control animals, epinephrine and th
e general beta-adrenergic agonist isoproterenol increased alveolar liq
uid clearance to similar to 50% of instilled volume (P < 0.05), wherea
s the beta(2)-adrenergic agonist terbutaline was without effect. The s
timulation of alveolar liquid clearance by epinephrine or isoprotereno
l was completely inhibited by the addition of the general beta-adrener
gic inhibitor propranolol or the beta(1)-adrenergic inhibitor atenolol
. Alveolar liquid clearance was inhibited by the sodium-channel inhibi
tor 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 vitr
o incubated lung tissue. The results suggest that alveolar liquid clea
rance in guinea pigs is mediated partly through amiloride-sensitive so
dium channels and that alveolar liquid clearance can be increased by s
timulation of primarily beta(1)-adrenergic receptors.