Document Detail

Alpha-adrenoceptor blockade modifies neurally induced atrial arrhythmias.
MedLine Citation:
PMID:  18716036     Owner:  NLM     Status:  MEDLINE    
Our objective was to determine whether neuronally induced atrial arrhythmias can be modified by alpha-adrenergic receptor blockade. In 30 anesthetized dogs, trains of five electrical stimuli (1 mA; 1 ms) were delivered immediately after the P wave of the ECG to mediastinal nerves associated with the superior vena cava. Regional atrial electrical events were monitored with 191 atrial unipolar electrodes. Mediastinal nerve sites were identified that reproducibly initiated atrial arrhythmias. These sites were then restimulated following 1 h (time control, n = 6), or the intravenous administration of naftopidil (alpha(1)-adrenergic blocker: 0.2 mg/kg, n = 6), yohimbine (alpha(2)-adrenergic blocker: 1 mg/kg, n = 6) or both (n = 8). A ganglionic blocker (hexamethonium: 1 mg/kg) was tested in four dogs. Stimulation of mediastinal nerves sites consistently elicited atrial tachyarrhythmias. Repeat stimulation after 1 h in the time-control group exerted a 19% decrease of the sites still able to induce atrial tachyarrhythmias. Hexamethonium inactivated 78% of the previously active sites. Combined alpha-adrenoceptor blockade inactivated 72% of the previously active sites. Bradycardia responses induced by mediastinal nerve stimulation were blunted by hexamethonium, but not by alpha(1,2)-adrenergic blockade. Naftopidil or yohimbine alone eliminated atrial arrhythmia induction from 31% and 34% of the sites (similar to time control). We conclude that heterogeneous activation of the intrinsic cardiac nervous system results in atrial arrhythmias that involve intrinsic cardiac neuronal alpha-adrenoceptors. In contrast to the global suppression exerted by hexamethonium, we conclude that alpha-adrenoceptor blockade targets intrinsic cardiac local circuit neurons involved in arrhythmia formation and not the flow-through efferent projections of the cardiac nervous system.
Louis-Philippe Richer; Alain Vinet; Teresa Kus; René Cardinal; Jeffrey L Ardell; John Andrew Armour
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2008-08-20
Journal Detail:
Title:  American journal of physiology. Regulatory, integrative and comparative physiology     Volume:  295     ISSN:  0363-6119     ISO Abbreviation:  Am. J. Physiol. Regul. Integr. Comp. Physiol.     Publication Date:  2008 Oct 
Date Detail:
Created Date:  2008-10-03     Completed Date:  2008-12-04     Revised Date:  2013-06-05    
Medline Journal Info:
Nlm Unique ID:  100901230     Medline TA:  Am J Physiol Regul Integr Comp Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  R1175-80     Citation Subset:  IM    
Centre de Recherche, Hôpital du Sacré-Coeur de Montréal, Montréal, Canada.
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MeSH Terms
Adrenergic alpha-1 Receptor Antagonists
Adrenergic alpha-2 Receptor Antagonists
Adrenergic alpha-Antagonists / pharmacology*
Arrhythmia, Sinus / physiopathology
Arrhythmias, Cardiac / physiopathology*
Atrial Appendage / physiopathology
Atrial Fibrillation / physiopathology
Atrial Flutter / physiopathology
Bradycardia / physiopathology
Electric Stimulation
Heart / drug effects*,  innervation,  physiopathology
Heart Atria / drug effects,  innervation,  physiopathology
Hexamethonium / pharmacology
Naphthalenes / pharmacology
Piperazines / pharmacology
Receptors, Adrenergic, alpha / physiology*
Receptors, Adrenergic, alpha-1 / physiology
Tachycardia / physiopathology
Tachycardia, Sinus / physiopathology
Vena Cava, Superior / physiology
Yohimbine / pharmacology
Grant Support
Reg. No./Substance:
0/Adrenergic alpha-1 Receptor Antagonists; 0/Adrenergic alpha-2 Receptor Antagonists; 0/Adrenergic alpha-Antagonists; 0/Naphthalenes; 0/Piperazines; 0/Receptors, Adrenergic, alpha; 0/Receptors, Adrenergic, alpha-1; 146-48-5/Yohimbine; 60-26-4/Hexamethonium; R9PHW59SFN/naftopidil

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