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J A Quest

Publications and source records attributed to J A Quest.

12 recordsLinked to original sources
PubMed1978

Effects of serotonin antagonists on digitalis-induced ventricular arrhythmias.

The present study was performed to determine whether pharmacological blockade of serotonin receptors would counteract digitalis-induced ventricular arrhythmias. The effect of the serotonin receptor blocking drugs, methysergide, cinansersin, and cyproheptadine on ventricular arrhythmias produced by ouabain was studied in anesthetized dogs. Each of the three serotonin receptor blocking drugs given as a bolus i.v. injection of 1.5--3.0 mg/kg produced an antiarrhythmic effect. In addition, methysergide administered in the above doses to cats intoxicated with deslanoside, restored an abnormal ventricular arrhythmia to either sinus or junctional rhythm. Methysergide, administered to cats intoxicated with deslanoside but pretreated with p-chlorophenylalanine, exerted an antiarrhythmic effect in less than half of the animals tested. These data indicate that serotonin antagonists are effective in counteracting digitalis-induced ventricular arrhythmias and support the notion that a serotonergic mechanism may be mediating the arrhythmogenic effect of digitalis.

Animals↗
PubMed1976

Effect of dihydro-ouabain on vascular tone on the perfused cannine hindlimb.

Digitalis compounds are known to cause contraction of vascular smooth muscle. However, it has been reported by Kahn and colleagues (J. Pharmacol. Exp. Ther. 142: 215-222, 1963) that dihydro-ouabain has no effect on vascular tone in dogs. The purpose of our study was to reassess the vasoconstrictor activity of dihydro-ouabain. This was done by monitoring perfusion pressure of the canine hindlimb preparation perfused at a constant rate of blood flow and administering intra-arterial injections of dihydro-ouabain. Increasing doses of this drug (i.e., 25, 50, 100, 200 and 300 mug) produced significant dose-dependent increases in perfusion pressure. Pretreatment with phentolamine prevented the effect of dihydro-ouabain on perfusion pressure. These results indicate that dihydro-ouabain causes contraction of vascular smooth muscle by an adrenergic mechanism.

Animals↗
PubMed1975

Neural mechanisms involved in acetylstrophanthidin-induced bradycardia.

The role of neural sites in the bradycardia produced by acetylstrophanthidin (14.1, 22.5 and 35.5 mug/kg) was studied in chloralose-anesthetized cats with efferent vagal tone blocked by atropine. The sites were: carotid sinus baroreceptors, aortic arch baroreceptors, cardiac sensory receptors, nodose ganglion receptors and central nervous system structures. The role of each site was determined by selective ablation of all sites except the one under study. Significant slowing in heart rate occurred when: 1) only carotid sinus baroreceptors were intact; 2) only aortic arch baroreceptors were intact and 3) only cardiac sensory receptors were intact. No cardiac slowing was observed when only nodose ganglion receptors, central sympathoinhibitory sites and beta adrenergic receptors were intact. These results indicate that in atropine-treated cats, the further slowing in heart rate produced by acetylstrophanthidin arises from activation of reflex sites located in the carotid sinus, aortic arch and myocardium.

Animals↗