Circulation, Vol 82, 951-964, Copyright © 1990 by American Heart Association
S Imaizumi, T Mazgalev, LS Dreifus, EL Michelson, A Miyagawa, S Bharati and M Lev
The mechanisms responsible for slowing cardiac impulse conduction through
the atrioventricular (AV) node are not well understood but include
anatomical architecture, presence of cells with diverse
electrophysiological characteristics, and modulation by autonomic nervous
system. The present study was designed to determine the site of vagally
induced slowing of conduction through the AV node. We attempted to
correlate the electrophysiological response of AV nodal cells to
postganglionic vagal stimulation applied in different regions of the node
with the morphological findings and patterns of
acetylcholinesterase-positive staining of nodal tissue. This multifaceted
approach revealed that vagal stimulation produced localized
hyperpolarization of the cells from the N region of the AV node, which
correlated with the strong acetylcholinesterase positive staining of the
central nodal area. In contrast, the density of the acetylcholinesterase
staining decreased toward both the AN and His bundle regions, whereas vagal
stimulation had a negligible effect on the cells from these regions. These
results suggest that vagal-induced depression of AV nodal conduction is
produced by release of acetylcholine predominantly around the midnodal
region and the depressive action of acetylcholine is concentrated on the
cells occupying the same region (i.e., the N cells). Thus, there appears to
be a close juxtaposition of nerve elements and effector cells in the
midnodal region of the AV node. This unique combination of available
neuromediator and responding cells with hyperpolarization and depressed
action potential determines the midnodal region as the focus of vagal
effect on AV nodal conduction.
ARTICLES
Morphological and electrophysiological correlates of atrioventricular nodal response to increased vagal activity
Department of Medicine, Lankenau Hospital, Philadelphia, PA 19151.
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