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Tachycardia during coronary occlusion is initiated by receptors in or near the heart, with the magnitude of the response depending on both cardiac receptors and arterial baroreceptors.
Reflex increases in heart rate which occurred during 1-minute occlusions of the left circumflex coronary artery were studied in conscious dogs. The results indicated that occlusion produced tachycardia (latency to onset 8.5 seconds) preceded by a rise in left atrial pressure (7.2 seconds) and followed by a small fall in arterial pressure (19.5 seconds). Bilateral baroreceptor denervation indicated that the onset of the changes in heart rate could not be accounted for by subtle baroreceptor sensitivity, although the peak response was much reduced (from 34.0 beats/min to 17.5 beats/min), indicating that the magnitude of the response did depend on intact baroreceptors. Beta-receptor blockade with propranolol or cardiac sympathectomy reduced the peak response from 34.0 beats/min to 16.1 beats/min or 12.2 beats/min, respectively. Vagal blockade with atropine reduced the response to 5.3 beats/min, indicating that the remainder of the response was carried in the vagus. Responses were much reduced after baroreceptor denervation plus β-receptor blockade (5.2 beats/min), indicating that the efferent vagal branch of the reflex originated primarily in the arterial baroreceptors. Tachycardia during coronary occlusion, then, is initiated by receptors in or near the heart, and the magnitude of the response is a combination response from these receptors and the arterial baroreceptors.
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Peterson et al. (1973) studied this question.
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