Active transport of sodium has been shown to be the predominant mechanism i
nvolved in alveolar liquid clearance. One regulatory mechanism involved in
the modulation of this transport system is cAMP. Although it was initially
thought that cAMP could directly modulate transepithelial Na+ transport, re
cent data suggest that this GAMP modulation could be secondary to the produ
ction of arachnidonic acid metabolites. The purpose of this study was thus
to evaluate if prostaglandin products could have an indirect or direct role
to play in lung liquid clearance. Addition of 10(-5) M salmeterol, known t
o increase intracellular cAMP, to the instilled fluid in rats stimulated lu
ng liquid clearance. However, addition of indomethacin did not influence th
e stimulating effect of salmeterol. Furthermore, addition of prostaglandin
E-2 to the instilled fluid did not stimulate alveolar fluid clearance. In o
rder to determine if this response could be species related, me evaluated i
f indomethacin could modulate alveolar liquid clearance in sheep. Presence
of cAMP and aminophylline stimulated lung liquid clearance in sheep, bat in
domethacin did not inhibit this response. The present study demonstrates th
at cyclooxygenase products are not involved in the modulation of basal or s
timulated alveolar or lung liquid clearance in sheep or rats.