TY - JOUR T1 - AN INITIAL DEPRESSION OF HEART RATE IN RESPONSE TO EPINEPHRINE IN HUMAN SUBJECTS JF - Journal of Pharmacology and Experimental Therapeutics JO - J Pharmacol Exp Ther SP - 143 LP - 152 VL - 63 IS - 2 AU - ROBERT T. FUCHS Y1 - 1938/06/01 UR - http://jpet.aspetjournals.org/content/63/2/143.abstract N2 - 1. The heart rate and blood pressure reactions to intravenous injections of epinephrine (0.025 mgm.) were studied in 40 male subjects (20 normals and 20 schizophrenics). Continuous records of the heart rate were obtained by means of a cardiochronograph. The features of the reaction considered in this paper were practically identical for both schizophrenic and normal subjects. 2. The heart rate reaction to epinephrine showed three distinct phases: (a) initial depression, (b) acceleration followed by (c) a second depression. 3. In another series of tests the reaction to epinephrine was studied after intravenous administration of 1 mgm. of atropine sulphate. Under such conditions the initial depression was reduced, on the average, by 72 per cent of its previous value. 4. The phase of acceleration represents the well known effect of epinephrine on the sympathetic nervous system. The final depressive phase is considered as a vagal effect. This is brought about by a reflex excitation of the cardio-inhibitory center from the carotid sinus and the sensitive zones of the aorta in response to the rise of blood pressure. 5. The initial depressive phase is of vagal origin, but is independent of the change in blood pressure. 6. For the explanation of the initial depressive phase two alternative hypotheses are offered: (a) one could assume a direct effect of epinephrine on either the cardio-inhibitory nerve endings or on the cardio-inhibitory center itself. There is, however, little factual evidence to favor such an assumption. (b) It seems more probable that the initial depression of heart rate represents a compensatory parasympathetic reaction to the sympathetic excitation. Such a mechanism might be mediated by higher regulatory centers in the diencephalon. This hypothesis, however, requires further testing. ER -