Document Detail

Ganglionated plexi modulate extrinsic cardiac autonomic nerve input: effects on sinus rate, atrioventricular conduction, refractoriness, and inducibility of atrial fibrillation.
MedLine Citation:
PMID:  17601547     Owner:  NLM     Status:  MEDLINE    
OBJECTIVES: This study sought to systematically investigate the interactions between the extrinsic and intrinsic cardiac autonomic nervous system (ANS) in modulating electrophysiological properties and atrial fibrillation (AF) initiation. BACKGROUND: Systematic ganglionated plexi (GP) ablation to evaluate the extrinsic and intrinsic cardiac ANS relationship has not been detailed. METHODS: The following GP were exposed in 28 dogs: anterior right GP (ARGP) near the sinoatrial node, inferior right ganglionated plexi (IRGP) at the junction of the inferior vena cava and atria, and superior left ganglionated plexi (SLGP) near the junction of left superior pulmonary vein and left pulmonary artery. With unilateral vagosympathetic trunk stimulation (0.6 to 8.0 V, 20 Hz, 0.1 ms in duration), sinus rate (SR), and ventricular rate (VR) during AF were compared before and after sequential ablation of SLGP, ARGP, and IRGP. RESULTS: The SLGP ablation significantly attenuated the SR and VR slowing responses with right or left vagosympathetic trunk stimulation. Subsequent ARGP ablation produced additional effects on SR slowing but not VR slowing. After SLGP + ARGP ablation, IRGP ablation eliminated VR slowing but did not further attenuate SR slowing with vagosympathetic trunk stimulation. Unilateral right and left vagosympathetic trunk stimulation shortened the effective refractory period and increased AF inducibility of atrium and pulmonary vein near the ARGP and SLGP, respectively. The ARGP ablation eliminated ERP shortening and AF inducibility with right vagosympathetic trunk stimulation, whereas SLGP ablation eliminated ERP shortening but not AF inducibility with left vagosympathetic trunk stimulation. CONCLUSIONS: The GP function as the "integration centers" that modulate the autonomic interactions between the extrinsic and intrinsic cardiac ANS. This interaction is substantially more intricate than previously thought.
Yinglong Hou; Benjamin J Scherlag; Jiaxiong Lin; Ying Zhang; Zhibing Lu; Kim Truong; Eugene Patterson; Ralph Lazzara; Warren M Jackman; Sunny S Po
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2007-06-18
Journal Detail:
Title:  Journal of the American College of Cardiology     Volume:  50     ISSN:  1558-3597     ISO Abbreviation:  J. Am. Coll. Cardiol.     Publication Date:  2007 Jul 
Date Detail:
Created Date:  2007-07-02     Completed Date:  2007-08-09     Revised Date:  2007-12-03    
Medline Journal Info:
Nlm Unique ID:  8301365     Medline TA:  J Am Coll Cardiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  61-8     Citation Subset:  AIM; IM    
Department of Cardiology, Shandong Provincial Qianfoshan Hospital, Clinical Medical College of Shandong University, Jinan City, Shandong, China.
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MeSH Terms
Atrial Fibrillation / etiology,  physiopathology*
Autonomic Pathways / physiopathology
Disease Models, Animal
Electric Stimulation / adverse effects
Electrodes, Implanted
Electrophysiologic Techniques, Cardiac / methods
Ganglia, Autonomic / physiopathology*
Heart Atria / innervation,  physiopathology*
Heart Conduction System / physiopathology*
Sensitivity and Specificity
Sinoatrial Node / physiopathology
Grant Support

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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