Abstract
Summary
Serotonin (10-500 μg) was infused into the pulmonary circulation of anesthetized, spontaneously breathing dogs and the effect on pulmonary hemodynamics [pulmonary artery pressure (P pa), left atrial pressure (P la), the pulmonary artery-left atrial pressure gradient (P pa-P la)] and pulmonary mechanics [pulmonary resistance (R L) and compliance (C L)] was determined. Pulmonary arterial hypertension, manifested by an increase in P pa and P pa-Pla with no change in P la, was caused by small doses of serotonin (30-100 μg) which had no measurable effect on R l and C l. These findings are consistent with the hypothesis that serotonin causes pulmonary arterial hypertension as a result of active pulmonary vasoconstriction rather than as a result of changes in the mechanical properties of the lungs.
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