AJP - Heart and Circulatory Physiology, Vol 256, Issue 3 859-H866, Copyright © 1989 by American Physiological Society
Subendocardial infarction produces epicardial parasympathetic denervation in canine left ventricle
J. B. Martins, R. Lewis, D. Wendt, D. D. Lund and P. G. Schmid
Department of Internal Medicine, University of Iowa, Iowa City.
Forty dogs underwent anterior descending coronary artery dissection with
most having occlusion that was either maintained or reperfused. Study was
performed 1-4 days later. Multiple electrodes placed in normal and ischemic
zones were used to determine the depth of the epicardial rim overlying a
subendocardial infarction. This was done by comparing voltage differential
with respect to time (dV/dt) measurements of sequential bipolar
electrograms along each needle. By this means, test sites with a rim were
documented, and depths of epicardial biopsies for choline acetyltransferase
were chosen. Epicardial effective refractory period (ERP) responses to
vagal nerve stimulation were measured. In sham-operated controls, vagal
stimulation prolonged ERP, and choline acetyltransferase activity was
equivalent in all sites. In contrast, dogs with all durations of coronary
occlusion and various thicknesses of subendocardial infarction had no
significant prolongation of ERP limited to rim sites overlying the infarct
during vagal nerve stimulation. Corresponding choline acetyltransferase
activity was decreased in rim sites compared with remote areas. In
addition, dogs given norepinephrine or physostigmine (to potentiate
parasympathetic responses) did not demonstrate significant ERP prolongation
with vagal stimulation. Infusion of acetylcholine into the distal ligated
coronary artery produced dose-dependent prolongation of ERP in sites
overlying the infarct. These data taken together support the hypothesis
that subendocardial infarction, regardless of its homogeneity or thickness,
produces parasympathetic denervation of the overlying epicardial rim.
