HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 295/4/R1175    most recent 00840.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Richer, L.-P. Articles by Armour, J. A. Search for Related Content PubMed PubMed Citation Articles by Richer, L.-P. Articles by Armour, J. A.

NEUROHUMORAL CONTROL OF CARDIOVASCULAR FUNCTION

-Adrenoceptor blockade modifies neurally induced atrial arrhythmias

¹Centre de Recherche, Hôpital du Sacré-Cœur de Montréal, Montréal, Canada; ²Department of Pharmacology, Faculty of Medicine, Université de Montréal, Montréal, Canada; ³Department of Physiology, Faculty of Medicine, Université de Montréal, Montréal, Canada; and ⁴Department of Pharmacology, East Tennessee State University, James H. Quillen College of Medicine, Johnson City, Tennessee

Submitted 21 November 2007 ; accepted in final form 13 August 2008

Our objective was to determine whether neuronally induced atrial arrhythmias can be modified by -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 (₁-adrenergic blocker: 0.2 mg/kg, n = 6), yohimbine (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 -adrenoceptor blockade inactivated 72% of the previously active sites. Bradycardia responses induced by mediastinal nerve stimulation were blunted by hexamethonium, but not by _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 -adrenoceptors. In contrast to the global suppression exerted by hexamethonium, we conclude that -adrenoceptor blockade targets intrinsic cardiac local circuit neurons involved in arrhythmia formation and not the flow-through efferent projections of the cardiac nervous system.

neuromodulation; cardiac nervous system; ganglionic blockade

This article has been cited by other articles:

				J. L. Ardell, R. Cardinal, M. Vermeulen, and J. A. Armour Dorsal spinal cord stimulation obtunds the capacity of intrathoracic extracardiac neurons to transduce myocardial ischemia Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2009; 297(2): R470 - R477. [Abstract] [Full Text] [PDF]