Circulation, Vol 72, 623-631, Copyright © 1985 by American Heart Association
MJ Barber, TM Mueller, BG Davies, RM Gill and DP Zipes
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 micrograms) and nicotine
(50 micrograms) 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 less than .01 vs preapplication values), while
topical nicotine produced a maximal depressor response of 14 +/- 2 mm Hg (p
less than .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.(ABSTRACT TRUNCATED AT 250 WORDS)
ARTICLES
Interruption of sympathetic and vagal-mediated afferent responses by transmural myocardial infarction
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