Effects of Serotonin on the Cardiopulmonary Circulatory System With and Without 5-HT2-Receptor Blockade by Ketanserin

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Abstract
Pulmonary embolism may cause pulmonary hypertension by mechanical obstruction, which might be amplified by vasoconstriction induced by serotonin released from the emboli. The purpose of the present study was to examine whether 5-HT2-receptors are involved in serotonin-induced pulmonary hypertension. Ketanserin was used as 5-HT2-serotoncrgic antagonist. In nine anesthetized mongrel dogs, the effect of serotonin infusions (10, 50, 100 μg/kg ± min) on mean pulmonary artery pressure (PAP), pulmonary vascular resistance (PVR), cardiac output (CO), stroke volume (SV), cardiac contractility (dP/dtmas), heart rate (HR), and mean aortic pressure (PAP) was studied with and without treatment by ketanserin (20 and 100 μg/kg). Serotonin caused dose-dependent increase in PAP, PVR, CO, SV, and dP/dtmas. A dose of 20 μg/kg ketanserin did not affect hemodynamics significantly, whereas 100 μg/kg of the compound significantly reduced PAP, TPR, and left ventricular dP/dtmas. The serotonin-induced increases in PAP, PVR, dP/dtmas CO, and SV were reduced significantly by 100 μg/kg ketanserin: the lower dose of ketanserin had only a slight blocking effect. Ketanserin blocks serotonin-induced pulmonary vasoconstriction partly. but it seems also to antagonize the positive inotropic effect of the monoamine.

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