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Hemodynamic effects of the serotonergic agent quipazine in the anesthetized dog
Author(s) -
Vidrio Horacio,
Mena Marco A.
Publication year - 1984
Publication title -
drug development research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.582
H-Index - 60
eISSN - 1098-2299
pISSN - 0272-4391
DOI - 10.1002/ddr.430040607
Subject(s) - methysergide , quipazine , anesthesia , bradycardia , medicine , cardiac output , vascular resistance , heart rate , blood pressure , hemodynamics , stroke volume , reflex bradycardia , chronotropic , serotonergic , serotonin , receptor
The hemodynamic effects of quipazine, a serotonergic agent, were determined in pentobarbital‐anesthetized, open‐chest dogs administering the drug IV, either by bolus injection or by continuous infusion. Bolus injections of 0.1 and 1 mg/kg elicited transient increases in blood pressure, peripheral resistance, aortic flow, and stroke volume. Administration of 10 mg/kg decreased blood pressure, aortic flow, heart rate, cardiac contractility, and venous pressure, and increased stroke volume. Infusion of quipazine at a rate of 0.5 mg/kg/min for 30 min initially increased blood pressure and peripheral resistance and subsequently produced hypotension and decreased cardiac function. From the beginning of infusion, heart rate and venous pressure decreased, while stroke volume increased. Pretreatment with methysergide antagonized the hypotension and bradycardia, as well as the changes in venous pressure and stroke volume. It was concluded that quipazine elicits complex, dose‐related cardiovascular effects, some of which (hypotension, venodilatation, bradycardia) are mediated through methysergide‐sensitive central serotonin receptors. The arterial vasoconstriction produced by low doses of the drug was not mediated through these receptors and was probably the result of activation of a cardiogenic reflex.