title: Ganglionated plexi modulate extrinsic cardiac autonomic nerve input: effects on sinus rate, atrioventricular conduction, refractoriness, and inducibility of atrial fibrillation.
abstract: OBJECTIVE
  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.
authors.affiliation: Department of Cardiology, Shandong Provincial Qianfoshan Hospital, Clinical Medical College of Shandong University, Jinan City, Shandong, China.
authors.forename: Yinglong
authors.initials: Y
authors.lastname: Hou
authors.forename: Benjamin J
authors.initials: BJ
authors.lastname: Scherlag
authors.forename: Jiaxiong
authors.initials: J
authors.lastname: Lin
authors.forename: Ying
authors.initials: Y
authors.lastname: Zhang
authors.forename: Zhibing
authors.initials: Z
authors.lastname: Lu
authors.forename: Kim
authors.initials: K
authors.lastname: Truong
authors.forename: Eugene
authors.initials: E
authors.lastname: Patterson
authors.forename: Ralph
authors.initials: R
authors.lastname: Lazzara
authors.forename: Warren M
authors.initials: WM
authors.lastname: Jackman
authors.forename: Sunny S
authors.initials: SS
authors.lastname: Po
mesh_terms: D000818:Animals; D001281:Atrial Fibrillation / Q000209:etiology / Q000503:physiopathology*; D017776:Autonomic Pathways / Q000503:physiopathology; D004195:Disease Models, Animal; D004285:Dogs; D004558:Electric Stimulation / Q000009:adverse effects; D004567:Electrodes, Implanted; D022062:Electrophysiologic Techniques, Cardiac / Q000379:methods; D005725:Ganglia, Autonomic / Q000503:physiopathology*; D006325:Heart Atria / Q000294:innervation / Q000503:physiopathology*; D006329:Heart Conduction System / Q000503:physiopathology*; D011336:Probability; D012680:Sensitivity and Specificity; D012849:Sinoatrial Node / Q000503:physiopathology