title: Low-level ganglionated plexus stimulation facilitates atrial fibrillation: in vivo and in vitro studies.
abstract: OBJECTIVE
  The purpose of the present study was to investigate whether long term low level autonomic activation can form electrophysiological substrate for atrial fibrillation (AF).
  
  
  RESULTS
  In 16 anesthetized open-chest dogs, electrodes on the anterior right ganglionated plexuses (GP) and superior left GP allowed 6-h low-level GP stimulation (LL-GPS) inducing a 10% decrease in sinus rate. Similar low-level stimulation (without myocardial capture) was delivered to the myocardium remote from the GP for 6h in another 16 dogs as control group. LL-GPS: a) induced shortening of the atrial effective refractory period and increase of the window of vulnerability for AF; b) significantly increased acetylcholine-regulated potassium current (I(KACh)) at left superior pulmonary vein (LSPV) while reduced the density of L-type calcium current (I(CaL)) at LSPV and both atria, the protein expression of the channel subunit showed a consistent alteration, however both without significant changes in mRNA level.
  
  
  CONCLUSIONS
  Six-hour LL-GPS induced significant changes in atrial electrophysiology and facilitated the initiation of AF, indicating that long-term low level autonomic activation would form electrophysiological substrate for AF. The underlying mechanism may be associated with a post-transcriptional regulation of increased I(KACh) and decreased I(CaL).
authors.affiliation: Department of Cardiology, Renmin Hospital of Wuhan University, PR China.
authors.forename: Liu
authors.initials: L
authors.lastname: Wu
authors.forename: Zhibing
authors.initials: Z
authors.lastname: Lu
authors.forename: Hong
authors.initials: H
authors.lastname: Jiang
authors.forename: Bo
authors.initials: B
authors.lastname: He
authors.forename: Wenbo
authors.initials: W
authors.lastname: He
authors.forename: Bo
authors.initials: B
authors.lastname: Cui
authors.forename: Xiaorong
authors.initials: X
authors.lastname: Hu
authors.forename: Congxin
authors.initials: C
authors.lastname: Huang
mesh_terms: D000109:Acetylcholine / Q000502:physiology; D000818:Animals; D001281:Atrial Fibrillation / Q000503:physiopathology*; D015153:Blotting, Western; D020746:Calcium Channels, L-Type / Q000502:physiology; D004285:Dogs; D004558:Electric Stimulation; D022062:Electrophysiologic Techniques, Cardiac; D055724:Electrophysiological Phenomena; D005071:Evoked Potentials / Q000502:physiology; D005725:Ganglia, Autonomic / Q000502:physiology*; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases / Q000096:biosynthesis; D006321:Heart / Q000502:physiology; D006325:Heart Atria / Q000503:physiopathology; D066298:In Vitro Techniques; D018727:Muscarinic Antagonists / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D015221:Potassium Channels / Q000502:physiology; D012313:RNA / Q000096:biosynthesis / Q000235:genetics; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D011976:Receptors, Muscarinic / Q000502:physiology; D012032:Refractory Period, Electrophysiological
chemical_list: D020746:Calcium Channels, L-Type; D018727:Muscarinic Antagonists; D015221:Potassium Channels; D012333:RNA, Messenger; D011976:Receptors, Muscarinic; D012313:RNA; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases; D000109:Acetylcholine