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Biomedical subjects

J A Quest

Publications and source records attributed to J A Quest.

44 records · Page 3Linked to original sources
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↗
PubMedDate not supplied

Effect of phenytoin on cardiac slowing induced by cholinergic stimulation.

Phenytoin was tested for its ability to counteract cholinergic-induced slowing in sinus rate in chloralose-anesthetized cats subjected to bilateral cervical vagotomy and spinal cord transection. The cholinergic stimuli consisted of electrical stimulation of the cervical vagus nerves and injected acetylcholine. Phenytoin administered as a continuous infusion of 0.5 and 1.0 mg/kg/min was found to significantly reduce the cardiac slowing produced by both modes of cholinergic stimulation. Blockade of the acetylcholine response suggested that the inhibitory effect of phenytoin was on the postsynaptic membrane. Measurement of serum levels of phenytoin performed in selected experiments revealed that the anticholinergic effect corresponded to plasma levels in humans exposed to therapeutic doses of this agent.

Acetylcholine↗