Abstract
Experiments were performed in anesthetized open-chest dogs pretreated with beta adrenoceptor blocking agent. Electrical stimulation of the left cardiac sympathetic nerve resulted in an initial decrease in coronary blood flow followed by a considerable increase after cessation of the stimulation. Atropine and hemicholinium inhibited the poststimulatory rebound phenomenon and corresponding fall in coronary vascular resistance without affecting cardiac activities. Physostigmine potentiated the poststimulatory increase in coronary blood flow and associated bradycardia. Changes after atropine and physostigmine of the initial decrease were slight and statistically not significant. Both phentolamine and 6-hydroxydopamine abolished not only the initial decrease but also the poststimulatory increase in coronary blood flow. Dipyridamole significantly enhanced the poststimulatory increase, while aminophylline suppressed it. It was concluded that the poststimulatory increase in coronary blood flow may consist of reactive hyperemia resulting from the initial decrease and in addition of cholinergic overshoot caused by a withdrawal of the inhibition of acetylcholine release through alpha adrenoceptor activity.
Published Version
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