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PMID: 6478556 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. Research Support, U.S. Gov't, P.H.S.

Phenol topically applied to canine left ventricular epicardium interrupts sympathetic but not vagal afferents.

Circulation research ·Vol. 55 ·No. 4 ·1984-10-00 ·Pages 532-44

Barber MJ, Mueller TM, Davies BG, Zipes DP

Abstract

The intracardiac pathways carrying the cardiovascular reflex responses mediated by cardiac sympathetic and vagal afferent fibers were examined in this study. We investigated the response to epicardial applications of bradykinin (5 micrograms) and nicotine (50 micrograms) before and after regional epicardial applications of 85% phenol in chloralose anesthetized open-chest dogs. Bradykinin stimulated sympathetic afferents, while nicotine stimulated vagal afferents. Topical applications of phenol were used to interrupt these pathways. Before phenol encircling, bradykinin significantly increased--whereas nicotine significantly decreased--mean arterial blood pressure when applied at the same sites. After phenol, nicotine applied to all sites within and outside the phenol circle continued to decrease mean arterial pressure, whereas bradykinin applied to sites within the circle no longer increased mean arterial pressure. Removal of aortic and carotid baroreceptors did not significantly affect these responses. Painting horizontal stripes of phenol on the anterior and posterior left ventricular free wall basal to the site of bradykinin application eliminated the elevation in mean arterial pressure produced by bradykinin. Reapplication of bradykinin basal to the stripe restored its response. Phenol stripes eliminated the nicotine vasodepressor response only when the stripe was painted in the atrioventricular groove. When bradykinin and nicotine were injected via a nonocclusive intracoronary catheter, both drugs elicited an early depressor response (interrupted by vagotomy) and, in some animals a late pressor response (interrupted by stellectomy). Epicardial phenol encircling the flow distribution of the cannulated coronary artery interrupted most or all of the sympathetic afferents mediating pressor responses to bradykinin or nicotine, while leaving the depressor responses intact. The depressor responses were eliminated by applying phenol to the atrioventricular groove or by transecting the cervical vagi. These data suggest that sympathetic afferent fibers travel in the superficial subepicardium in an apex-to-base direction. Vagal afferent fibers travel deeper in the myocardium until they approach the atrioventricular groove, where they ascend to the superficial subepicardium.

MeSH Terms
Afferent Pathways/drug effects,physiology Animals Blood Pressure/drug effects Bradykinin/pharmacology Denervation Dogs Female Heart/drug effects,innervation Heart Rate/drug effects Male Neurons, Afferent/drug effects,physiology Nicotine/pharmacology Phenol Phenols/pharmacology Pressoreceptors/physiology Sympathetic Nervous System/physiology Vagus Nerve/physiology
Chemicals
Phenols Phenol Nicotine Bradykinin
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Barber M J
Mueller T M
Davies B G
Zipes D P
Article Info
Journal
Circulation research
Abbr.
Circ Res
ISSN
0009-7330
Published
1984-10-00
Pages
532-44
Language
English
Region
United States
NLM ID
0047103
Subset
IM
Grants
NHLBI NIH HHS · HL-06308 · United States
NHLBI NIH HHS · HL-07182 · United States
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