Differing sympathetic and vagal effects on atrial fibrillation in dogs: role of refractoriness heterogeneity

Am J Physiol. 1997 Aug;273(2 Pt 2):H805-16. doi: 10.1152/ajpheart.1997.273.2.H805.

Abstract

Although sympathetic activation is believed to promote atrial fibrillation (AF), the effects of sympathetic stimulation on AF have not been systematically studied. In seven morphine-chloralose-anesthetized dogs, autonomic decentralization increased atrial effective refractory period (ERP) and reentrant wavelength (WL) and decreased the duration of AF induced by burst atrial pacing. Graded bilateral stellate ansa stimulation decreased ERP and WL to values similar to those before decentralization but did not return AF duration to predecentralization values. Sympathetic and bilateral vagal stimulation were adjusted in six additional dogs to produce similar effects on ERP and WL. Despite comparable effects on mean WL, the duration of AF was increased by vagal stimulation from 14 +/- 5 (control) to 372 +/- 96 s (P < 0.001) but was not altered significantly (26 +/- 10 s) by sympathetic stimulation. Vagal stimulation increased the variability in atrial refractoriness, as indicated by the standard deviation of ERP at seven atrial sites and of activation frequency during AF at 112 recording sites, whereas sympathetic stimulation had no significant effect on these indexes of ERP heterogeneity. We conclude that sympathetic stimulation is much less effective than vagal stimulation in promoting AF and that heterogeneity in atrial ERP may be important in determining the ability to sustain AF.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Arrhythmia Agents / pharmacology
  • Atrial Fibrillation / physiopathology*
  • Atrial Function
  • Atropine / pharmacology
  • Dogs
  • Electric Stimulation
  • Female
  • Male
  • Nadolol / pharmacology
  • Refractory Period, Electrophysiological*
  • Sympathetic Nervous System / physiopathology*
  • Time Factors
  • Vagus Nerve / physiopathology*

Substances

  • Anti-Arrhythmia Agents
  • Nadolol
  • Atropine