Abstract
Summary and Conclusions
The actions of Dibenamine on the cardiovascular adjustments caused by epinephrine, acetylcholine, pitressin, and angiotonin have been studied in unanesthetized dogs. Dibenamine produced an increase in heart rate which persisted for one to 3 hours.
A test dose of epinephrine which regularly caused reflex cardiac slowing in normal unanesthetized dogs produced severe cardiac acceleration after administration of Dibenamine. This acceleration is attributable to the direct stimulatory action of epinephrine on the sino-auricular node and to reflex acceleration from a fall in blood pressure.
The compensatory cardiac acceleration produced by injection of a test dose of acetylcholine was undiminished and prolonged in unanesthetized animals under the influence of Dibenamine. This result is compatible with the interpretation that the vasoconstrictor mechanisms are impaired while the cardioaccelerator mechanisms are relatively intact.
The severe cardiac inhibition produced by pitressin and angiotonin in unanesthetized dogs, which is attributable to reflexes elicited by the rise in arterial blood pressure subsequent to vasoconstriction, was not prevented by Dibenamine.
The results of these experiments on unanesthetized dogs are in accord with the interpretations of Nickerson and Goodman 1 concerning the sites of action of Dibenamine.
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