AN ANALYSIS OF THE CAROTID SINUS CARDIOVASCULAR REFLEX MECHANISM

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Abstract
Expts. were carried out on nembutalized dogs in which the carotid sinus was vascularly isolated as a cul-de-sac and stimulated with a sudden increase of perfusion pressure to 220-240 mm. Hg. The vagal response as shown by cardiac slowing is most marked immediately following sinus distention; the bradycardia due to sympathetic inhibition appears slowly and becomes the major restraining influence as the vagal effect diminishes. The combined effect of vagal and sympathetic components is always greatest during the early moments of the stimulation period. By using animals in which the sympathetic nervous system is surgically removed or functionally excluded either by low cervical cord section or with dihydroergotamine (DHE45), it is demonstrated that vagal cardiac slowing is a discrete response and that it is not dependent on the sympathetic depression which normally invariably occurs in the carotid sinus reflex. It is shown that adaptation of the sino-vagal bradycardia may be influenced by the one or more of the following factors: a) adap-tation of the sinus pressoreceptors, b) aortic depressor nerve buffer mechanism, c) adaptation in centers of the brain stem and d) "vagal escape." In the sinus depressor reflex, there exists a balance between afferent and efferent vagal impulses; elimination of the former enhances the response whereas ex-clusion of the latter lessens it.

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