Document Detail

Morphological and electrophysiological correlates of atrioventricular nodal response to increased vagal activity.
MedLine Citation:
PMID:  2394013     Owner:  NLM     Status:  MEDLINE    
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.
S Imaizumi; T Mazgalev; L S Dreifus; E L Michelson; A Miyagawa; S Bharati; M Lev
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Publication Detail:
Type:  In Vitro; Journal Article    
Journal Detail:
Title:  Circulation     Volume:  82     ISSN:  0009-7322     ISO Abbreviation:  Circulation     Publication Date:  1990 Sep 
Date Detail:
Created Date:  1990-10-09     Completed Date:  1990-10-09     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  951-64     Citation Subset:  AIM; IM    
Department of Medicine, Lankenau Hospital, Philadelphia, PA 19151.
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MeSH Terms
Atrioventricular Node / metabolism,  pathology,  physiology*
Ganglia / physiology
Heart Conduction System / physiology*
Vagus Nerve / physiology*

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