PHYSIOLOGICAL PROPERTIES OF A CENTRAL EXCITATORY AGENT IN FLUID OBTAINED BY OCCIPITAL PUNCTURE OF MAN AND ANIMALS
- 30 September 1937
- journal article
- research article
- Published by American Physiological Society in American Journal of Physiology-Legacy Content
- Vol. 120 (2) , 392-400
- https://doi.org/10.1152/ajplegacy.1937.120.2.392
Abstract
Fluid obtained by occipital puncture from dogs before and after hypophysectomy, cats, goats and man. yields an extract which when injected into anesthetized cats produces physiological evidence of marked central excitation. If the vagi were intact the blood pressure fell and the heart was markedly slowed, and this was followed by a rise in pressure and increase in heart rate. If the vagi were severed, injection of C.E.A. (central excitatory agent) was associated with a sharp rise in blood pressure without significant change in heart rate. Simultaneously exophthalmos, retraction of the nictitating membrane and other evidences of excitation occurred. The excitation appeared to be mediated by the nervous system because injury to or removal of the C.N.S abolished the response; the response was rapidly fatigued; adrenalec-tomy, splanchnic nerve resection and carotid sinus dener-vation might modify somewhat but did not inhibit completely the response; and the response differed in several respects to peripherally acting substances such as epi-nephrine and tyramine. The pressor response was probably not due chiefly to epinephrine secreted by the adrenal glands because adrenalectomy altered but did not abolish the response; control periods of asphyxia did not duplicate the response; cocaine did not potentiate the response either of the blood vessels or the nictitating membrane; ergotoxine in doses sufficient to reverse the pressor response of epinephrine did not reverse that of C.E.A.; denervation of the nictitating membrane by superior cervical ganglionectomy abolished the immediate response to C.E.A. but sensitized it to epinephrine; and repeated doses of C.E.A. rapidly diminished the response of the mechanism responsible for the rise in arterial pressure contrary to the action of epinephrine.This publication has 2 references indexed in Scilit:
- STUDIES ON EXPERIMENTAL HYPERTENSIONThe Journal of Experimental Medicine, 1934
- STUDIES ON CONDITIONS OF ACTIVITY IN ENDOCRINE ORGANSAmerican Journal of Physiology-Legacy Content, 1932