Pulmonary inactivation of serotonin and site of serotonin pulmonary vasoconstriction.

To determine whether the site of serotonin-induced pulmonary vasoconstriction is influenced by serotonin uptake and inactivation within the lung, we utilized an isolated perfused left lower lobe of the dog lung, which could be perfused with flow in the normal direction (i.e., blood flowing into the lobar artery) or in the retrograde direction (i.e., blood flowing into the lobar vein). To localize the site of vasoconstriction, we utilized an outflow occlusion technique in which the changes in lobar vascular resistance were divided into changes in arterial and venous resistances. Serotonin infusion constricted vessels on the arterial side of the site of serotonin uptake during both forward and retrograde perfusion while having much less influence on the venous side. However, during retrograde perfusion the serotonin infusion rate required to produce a given increase in arterial resistance was approximately 85 micrograms/min greater than during forward perfusion. Thus, it would appear that serotonin was primarily an arterial constrictor in this preparation and that, although the lung removed a substantial quantity of serotonin, the uptake and inactivation within the lung had relatively little influence on the site of serotonin vasoconstriction.