Vagal stimulation promotes atrial electrical remodeling induced by rapid atrial pacing in dogs

Evidence of a noncholinergic effect

Donghui Yang, Yutao Xi, Tomohiko Ai, Geru Wu, Junping Sun, Mehdi Razavi, Scott Delapasse, Mossaib Shurail, Lianjun Gao, Nilesh Mathuria, MacArthur Elayda, Jie Cheng

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Background: Atrial electrical remodeling (AER) is one of the mechanisms by which atrial fibrillation (AF) begets AF. It is known that vagal activity increases the propensity for AF. However, vagal effects on AER have not been fully investigated. Methods: Adult mongrel dogs were divided in four groups: group I, rapid atria pacing (RAP); group II, RAP plus vagal nerve stimulation (VNS); group III, RAP and VNS with atropine (0.2 mg/kg/h, intravenous), and group IV, group III plus vasoactive intestinal polypeptide (VIP) antagonist ([D-p-Cl-Phe 6, Leu 17]-VIP, 0.125 μg/kg/h). VNS was performed bilaterally through vagosympathetic trunks to achieve second-degree AV block or sinus rate slowing of >30 beats per minute. Atrial effective refractory periods (AERPs) were determined in the coronary sinus and right atrial appendage every hour at drive cycle lengths (DCLs) 350 ms, 300 ms, and 250 ms. Results: During 5 hours RAP with or without VNS, AERP shortened progressively from baseline at both pacing sites and at all DCLs (P <0.01). Furthermore, RAP-induced AERP shortening was more pronounced with VNS (P <0.01). With atropine, the AERP shortening during VNS was blunted (P <0.01), but was still significantly more pronounced than that in group I (P <0.05). However, VNS effect on AERP shortening was eliminated completely with the combination of atropine and VIP antagonist (P = 0.15 vs group I). Conclusion: Increased vagal activity promotes RAP-induced AER, which could not be totally accounted for by cholinergic effect but could be blocked by the combination of atropine and VIP antagonist. Vagally released VIP may have important role in the vagal promotion of AER.

Original languageEnglish (US)
Pages (from-to)1092-1099
Number of pages8
JournalPACE - Pacing and Clinical Electrophysiology
Volume34
Issue number9
DOIs
StatePublished - Sep 2011
Externally publishedYes

Fingerprint

Atrial Remodeling
Vagus Nerve Stimulation
Dogs
Vasoactive Intestinal Peptide
Atropine
Atrial Fibrillation
Atrial Appendage
Coronary Sinus
Atrioventricular Block
Cholinergic Agents

Keywords

  • atrium
  • electrophysiology
  • remodeling
  • vagus nerve
  • vasoactive intestinal polypeptide

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Vagal stimulation promotes atrial electrical remodeling induced by rapid atrial pacing in dogs : Evidence of a noncholinergic effect. / Yang, Donghui; Xi, Yutao; Ai, Tomohiko; Wu, Geru; Sun, Junping; Razavi, Mehdi; Delapasse, Scott; Shurail, Mossaib; Gao, Lianjun; Mathuria, Nilesh; Elayda, MacArthur; Cheng, Jie.

In: PACE - Pacing and Clinical Electrophysiology, Vol. 34, No. 9, 09.2011, p. 1092-1099.

Research output: Contribution to journalArticle

Yang, Donghui ; Xi, Yutao ; Ai, Tomohiko ; Wu, Geru ; Sun, Junping ; Razavi, Mehdi ; Delapasse, Scott ; Shurail, Mossaib ; Gao, Lianjun ; Mathuria, Nilesh ; Elayda, MacArthur ; Cheng, Jie. / Vagal stimulation promotes atrial electrical remodeling induced by rapid atrial pacing in dogs : Evidence of a noncholinergic effect. In: PACE - Pacing and Clinical Electrophysiology. 2011 ; Vol. 34, No. 9. pp. 1092-1099.
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abstract = "Background: Atrial electrical remodeling (AER) is one of the mechanisms by which atrial fibrillation (AF) begets AF. It is known that vagal activity increases the propensity for AF. However, vagal effects on AER have not been fully investigated. Methods: Adult mongrel dogs were divided in four groups: group I, rapid atria pacing (RAP); group II, RAP plus vagal nerve stimulation (VNS); group III, RAP and VNS with atropine (0.2 mg/kg/h, intravenous), and group IV, group III plus vasoactive intestinal polypeptide (VIP) antagonist ([D-p-Cl-Phe 6, Leu 17]-VIP, 0.125 μg/kg/h). VNS was performed bilaterally through vagosympathetic trunks to achieve second-degree AV block or sinus rate slowing of >30 beats per minute. Atrial effective refractory periods (AERPs) were determined in the coronary sinus and right atrial appendage every hour at drive cycle lengths (DCLs) 350 ms, 300 ms, and 250 ms. Results: During 5 hours RAP with or without VNS, AERP shortened progressively from baseline at both pacing sites and at all DCLs (P <0.01). Furthermore, RAP-induced AERP shortening was more pronounced with VNS (P <0.01). With atropine, the AERP shortening during VNS was blunted (P <0.01), but was still significantly more pronounced than that in group I (P <0.05). However, VNS effect on AERP shortening was eliminated completely with the combination of atropine and VIP antagonist (P = 0.15 vs group I). Conclusion: Increased vagal activity promotes RAP-induced AER, which could not be totally accounted for by cholinergic effect but could be blocked by the combination of atropine and VIP antagonist. Vagally released VIP may have important role in the vagal promotion of AER.",
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T2 - Evidence of a noncholinergic effect

AU - Yang, Donghui

AU - Xi, Yutao

AU - Ai, Tomohiko

AU - Wu, Geru

AU - Sun, Junping

AU - Razavi, Mehdi

AU - Delapasse, Scott

AU - Shurail, Mossaib

AU - Gao, Lianjun

AU - Mathuria, Nilesh

AU - Elayda, MacArthur

AU - Cheng, Jie

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N2 - Background: Atrial electrical remodeling (AER) is one of the mechanisms by which atrial fibrillation (AF) begets AF. It is known that vagal activity increases the propensity for AF. However, vagal effects on AER have not been fully investigated. Methods: Adult mongrel dogs were divided in four groups: group I, rapid atria pacing (RAP); group II, RAP plus vagal nerve stimulation (VNS); group III, RAP and VNS with atropine (0.2 mg/kg/h, intravenous), and group IV, group III plus vasoactive intestinal polypeptide (VIP) antagonist ([D-p-Cl-Phe 6, Leu 17]-VIP, 0.125 μg/kg/h). VNS was performed bilaterally through vagosympathetic trunks to achieve second-degree AV block or sinus rate slowing of >30 beats per minute. Atrial effective refractory periods (AERPs) were determined in the coronary sinus and right atrial appendage every hour at drive cycle lengths (DCLs) 350 ms, 300 ms, and 250 ms. Results: During 5 hours RAP with or without VNS, AERP shortened progressively from baseline at both pacing sites and at all DCLs (P <0.01). Furthermore, RAP-induced AERP shortening was more pronounced with VNS (P <0.01). With atropine, the AERP shortening during VNS was blunted (P <0.01), but was still significantly more pronounced than that in group I (P <0.05). However, VNS effect on AERP shortening was eliminated completely with the combination of atropine and VIP antagonist (P = 0.15 vs group I). Conclusion: Increased vagal activity promotes RAP-induced AER, which could not be totally accounted for by cholinergic effect but could be blocked by the combination of atropine and VIP antagonist. Vagally released VIP may have important role in the vagal promotion of AER.

AB - Background: Atrial electrical remodeling (AER) is one of the mechanisms by which atrial fibrillation (AF) begets AF. It is known that vagal activity increases the propensity for AF. However, vagal effects on AER have not been fully investigated. Methods: Adult mongrel dogs were divided in four groups: group I, rapid atria pacing (RAP); group II, RAP plus vagal nerve stimulation (VNS); group III, RAP and VNS with atropine (0.2 mg/kg/h, intravenous), and group IV, group III plus vasoactive intestinal polypeptide (VIP) antagonist ([D-p-Cl-Phe 6, Leu 17]-VIP, 0.125 μg/kg/h). VNS was performed bilaterally through vagosympathetic trunks to achieve second-degree AV block or sinus rate slowing of >30 beats per minute. Atrial effective refractory periods (AERPs) were determined in the coronary sinus and right atrial appendage every hour at drive cycle lengths (DCLs) 350 ms, 300 ms, and 250 ms. Results: During 5 hours RAP with or without VNS, AERP shortened progressively from baseline at both pacing sites and at all DCLs (P <0.01). Furthermore, RAP-induced AERP shortening was more pronounced with VNS (P <0.01). With atropine, the AERP shortening during VNS was blunted (P <0.01), but was still significantly more pronounced than that in group I (P <0.05). However, VNS effect on AERP shortening was eliminated completely with the combination of atropine and VIP antagonist (P = 0.15 vs group I). Conclusion: Increased vagal activity promotes RAP-induced AER, which could not be totally accounted for by cholinergic effect but could be blocked by the combination of atropine and VIP antagonist. Vagally released VIP may have important role in the vagal promotion of AER.

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