Bolus injection of acetylcholine terminates atrial fibrillation in rats

Ilya A. Fleidervish, Yuri Goldberg, I. Eli Ovsyshcher

Research output: Contribution to journalArticlepeer-review

3 Scopus citations

Abstract

It is well established that a tonic increase in the availability of the atrial muscarinic K+ channels, either by enhanced vagal tone or by steady infusion of a low-dose of cholinergic or adenosine receptor agonists, promotes the genesis of atrial fibrillation. Here, we aimed to test the hypothesis that bolus administration of a muscarinic receptor agonist would destabilize and terminate atrial arrhythmia by uniformly and transiently activating K+ channels throughout the atria, and that if the agonist was rapidly hydrolysable, it would dissipate before the more tonic, pro-arrhythmic effects could take hold. The episodes of untreated atrial fibrillation, induced in anesthetized rats by programmed electrical stimulation via trans-esophageal bipolar catheter, lasted on average 8.6 ± 2.2 min (n = 32). Intravenous injection of a model hydrolysable muscarinic agonist, acetylcholine (0.2 mg/kg body weight), converted atrial fibrillation into sinus rhythm within 8.4 ± 1.9 s (n = 10, P < 0.05). The termination of an atrial fibrillation episode was always accompanied by transient bradycardia; the sinus rhythm gradually accelerated and reached pre-atrial fibrillation values within 10-20 s of injection. In conclusion, our evidence indicates that bolus administration of rapidly hydrolysable muscarinic agonist could be an effective way to pharmacologically terminate atrial fibrillation and restore sinus rhythm.

Original languageEnglish
Pages (from-to)326-329
Number of pages4
JournalEuropean Journal of Pharmacology
Volume579
Issue number1-3
DOIs
StatePublished - 28 Jan 2008
Externally publishedYes

Keywords

  • Acetylcholine
  • Anti-arrhythmic agents
  • Arrhythmia (mechanisms)
  • Defibrillation
  • K-channel

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