Interruption of sympathetic and vagal-mediated afferent responses by transmural myocardial infarction

M. J. Barber, T. M. Mueller, B. G. Davies, R. M. Gill, D. P. Zipes

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We have demonstrated previously that sympathetic and vagal afferents travel in an apical-to-basal course in the heart, and can be stimulated selectively with epicardial applications of bradykinin and nicotine, respectively. In this study we tested the hypothesis that transmural myocardial infarction interrupts sympathetic and vagal afferent fibers traveling through the infarction and produces regions of afferent denervation in areas apical to the infarction. In open-chest, chloralose-anesthetized dogs, transmural myocardial infarction was created by embolizing a diagonal branch of the left anterior descending coronary artery with a vinyl latex solution that was injected directly into the artery and hardened rapidly. The transmural nature of the infarction was verified by the nitro blue tetrazolium staining technique for dehydrogenase enzymes. Epicardial applications of bradykinin (5 μg) and nicotine (50 μg) were used to stimulate chemically sensitive sympathetic and vagal afferent nerve endings, respectively. Twenty-nine dogs were studied before and 90 min after creation of transmural myocardial infarction. In 20 dogs, epicardial bradykinin applied before production of transmural myocardial infarction produced a maximal pressor response of 13 ± 3 mm Hg 40 sec after application (p < .01 vs preapplication values), while topical nicotine produced a maximal depressor response of 14 ± 2 mm Hg (p < .01 vs preapplication values) 20 sec after application at all sites tested. Ninety minutes after production of transmural myocardial infarction, epicardial sites basal to the infarction continued to respond normally to both drugs, while sites within the area of infarction and apical to the area (noninfarcted myocardium) no longer showed a pressor response to topical bradykinin or a depressor response to topical nicotine. Nerve interruptions in 12 dogs demonstrated that the sympathetic afferent responses elicited by bradykinin were eliminated with bilateral stellectomy, while vagal afferent responses elicited by nicotine were interrupted by transection of the cervical vagi. In 10 dogs, more extensive epicardial mapping of responses to the two drugs revealed that sites were not always afferently denervated in a homogeneous manner. Several sites medial and apical to the transmural myocardial infarction continued to show pressure responses to bradykinin, but were unresponsive to topical nicotine. We conclude that transmural myocardial infarction produces areas of both sympathetic and vagal afferent denervation in infarcted and in noninfarcted myocardium apical to the region of infarction. This afferent denervation is not homogeneous in all areas.

Original languageEnglish (US)
Pages (from-to)623-631
Number of pages9
Issue number3
StatePublished - Jan 1 1985

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

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    Barber, M. J., Mueller, T. M., Davies, B. G., Gill, R. M., & Zipes, D. P. (1985). Interruption of sympathetic and vagal-mediated afferent responses by transmural myocardial infarction. Circulation, 72(3), 623-631.