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Journal of Pharmacology And Experimental Therapeutics, Vol. 112, Issue 2, 138-150, 1954
Copyright © 1954 by American Society for Pharmacology and Experimental Therapeutics


THE NATURE OF THE REFLEX VASODILATATION INDUCED BY EPINEPHRINE

Carl C. Gruhzit 1, Walter A. Freyburger 2, and Gordon K. Moe 1

1 Department of Physiology, State University of New York, Upstate Medical Center, Syracuse, and the Department of Pharmacology, University of Michigan, Ann Arbor
2 Department of Physiology, State University of New York, Upstate Medical Center, Syracuse, nd the Department of Pharmacology, University of Michigan, Ann Arbor

1. Vasodilatation occurring in the femoral vessels of anesthetized dogs following administration of epinephrine was found to be in part the expression of a reflex mechanism, previously undescribed.

2. The reflex is not prevented by denervation of the carotid sinuses and section of the vagi, nor by the use of a stabilizer limiting the pressor responses to epinephrine.

3. The reflex does not occur following injection of epinephrine into the aorta distal to the subclavian artery, even though the pressor response may exceed that resulting from intravenous administration.

4. The reflex is elicited by norepinephrine, though somewhat larger doses are required than with epinephrine; it is not observed following injection of phenylephrine ephrine or ephedrine in equipressor doses.

5. The reflex was shown not to be primarily due to activation of the receptors of the Bezold reflex, nor to alterations of mean pressure within the atria or the pulmonary vessels, nor to activation of chemoreceptors within the cardiac or pulmonary circulations.

6. Femoral vasodilatation was occasionally observed following injection of epinephrine into the brachiocephalic artery, but the magnitude of the response was always less than that evoked by intravenous injection.

7. Thoracic sympathectomy, alone or combined with vagotomy and carotid denervation, failed to prevent the reflex.

8. Application of dibucaine over the thoracic aorta diminished the reflex dilatation without abolishing other depressor reflexes.

9. Section of the thoracic dorsal roots completely abolished the reflex.

10. Mechanical exclusion of the descending thoracic aorta by suitable clamping procedures prevented the reflex response.

11. It is postulated that mechanoreceptors along the course of the thoracic aorta, activated by the inotropic cardiac action of epinephrine, may be the afferent source of the reflex.

12. Central connections and efferent pathways have not yet been studied.

Submitted on May 28, 1954







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Copyright © 1954 by the American Society for Pharmacology and Experimental Therapeutics.