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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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-serotonergic antagonist. In nine anesthetized mongrel dogs, the effect of serotonin infusions (10, 50, 100 micrograms/kg . min) on mean pulmonary artery pressure (PAP), pulmonary vascular resistance (PVR), cardiac output (CO), stroke volume (SV), cardiac contractility (dP/dtmax), heart rate (HR), and mean aortic pressure (PAO) was studied with and without treatment by ketanserin (20 and 100 micrograms/kg). Serotonin caused dose-dependent increase in PAP, PVR, CO, SV, and dP/dtmax. A dose of 20 micrograms/kg ketanserin did not affect hemodynamics significantly, whereas 100 micrograms/kg of the compound significantly reduced PAO, TPR, and left ventricular dP/dtmax. The serotonin-induced increases in PAP, PVR, dP/dtmax, CO, and SV were reduced significantly by 100 micrograms/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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PMID:Effects of serotonin on the cardiopulmonary circulatory system with and without 5-HT2-receptor blockade by ketanserin. 241 62

The release of platelet-derived vasoactive substances, particularly serotonin (5-HT), have been implicated in the pulmonary vasoconstrictor response following acute pulmonary embolism. Therefore, we studied the effects of infusing ketanserin, a 5-HT blocking agent, upon pulmonary and systemic hemodynamics and gas exchange in 10 patients with severe acute pulmonary embolism. These patients evidenced 45 +/- 17% mean angiographic pulmonary vascular obstruction. Ketanserin significantly decreased the mean pulmonary arterial pressure from 26 +/- 6 to 23 +/- 5 mm Hg (p less than 0.001). The total pulmonary vascular resistance decreased from 9.1 +/- 3.2 to 8.3 +/- 2.5 mm Hg/L X min X m2 (p less than 0.001). However, the mean cardiac index was unchanged. The systemic arterial and right atrial pressures were significantly decreased after ketanserin. The PaO2 increased in all patients from 60.5 +/- 12.6 to 66.5 +/- 13.6 mm Hg (p less than 0.05), whereas the venous admixture was unchanged. This was attributed to an increased PVO2 (27 +/- 7 to 30 +/- 5 mmHg, p less than 0.01) secondary to a reduction of calculated peripheral oxygen consumption during ketanserin infusion. The results indicate ketanserin is a mild pulmonary vasodilator and can reduce the pulmonary hypertension and increase the PaO2 after pulmonary embolism.
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PMID:Cardiopulmonary effects of ketanserin infusion in human pulmonary embolism. 380 Jan 40