Pulmonary venous responses to thromboxane A2 analogue and atrial natriuretic peptide in lambs.
To characterize pulmonary venous vasoactivity and the factors that modulate it, we determined venous responses to a vasoconstrictor agent, thromboxane A2 (TXA2) analogue U46619, and to a vasodilator agent, atrial natriuretic peptide (ANP), in 28 isolated blood-perfused lamb lungs under conditions of varying vascular tone and intraluminal pressures. TXA2 was given in a 5 micrograms/kg bolus followed by a steady infusion of 1 micrograms/kg/min to three groups of lungs: group 1, n = 4, with low vasomotor tone; group 2, n = 8, with moderate vasomotor tone; and group 3, n = 7, with moderate vasomotor tone and high venous intraluminal pressures. Group 3 lungs were reverse-perfused to obtain high venous pressures. ANP was given as two 10 micrograms/kg bolus injections, 5 minutes apart, to three groups of lungs: group 4, n = 4, with low vasomotor tone; group 5, n = 5, with moderate vasomotor tone; and group 6, n = 8, with high vasomotor tone. Group 6 lungs were vasoconstricted with TXA2 infusion. In all lungs, we measured blood flow and pressures in the pulmonary artery and left atrium and partitioned the venous segment by measuring pressures in 20-80-microns venules by micropuncture. We found that the venous constrictor response to TXA2 was greatest in lungs with moderate basal vasomotor tone and low venous intraluminal pressures. In lungs with low vasomotor tone or high venous intraluminal pressures, the venous response to TXA2 was attenuated. The vasodilator response to ANP was negligible in lungs with low vasomotor tone, probably because they were already maximally vasodilated, but similar in lungs with moderate and high vasomotor tone.(ABSTRACT TRUNCATED AT 250 WORDS)
- Copyright © 1990 by American Heart Association