Abstract
Recently we reported (1) that in the dog the cardiac effects produced by angiotensin were caused by stimulation of ganglia in the vicinity of the caudal cervical ganglia. Since it is generally assumed that the stellate ganglia and not the caudal cervical ganglia are the principal cardiac sympathetic ganglia, we devised experiments to verify our contention and to locate more precisely the major synapse of the sympathetic fibers in the dog that affect heart rate and right ventricular contractile force. These experiments consisted of stimulation of the sympathetic fibers at several sites along their pathway from the thoracic sympathetic trunk to a location near the heart, before and after complete ganglionic blackade.
Since Flacke and Gillis (2), and Trendelenburg (3), showed that nicotinic and muscarinic blocking agents are necessary to completely block ganglionic transmission, we also tested the effects of hexamethonium and atropine, alone or together, on ganglionic transmission in the intact open-chest dog preparation.
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