Abstract
Objective: To determine whether neurally induced atrial arrhythmias can be modified by α-adrenergic receptor blockade. Methods: In 24 anaesthetized dogs, trains of 5 electrical stimuli were delivered during the atrial refractory period to mediastinal nerves associated with the superior vena cava. Regional atrial electrical events were characterized using multiple unipolar electrodes. Active neural sites which induce atrial arrhythmias were identified and then re-stimulated following administration of naftopidil (α1-adrenergic blocker: 0.2 mg/kg iv) and/or yohimbine (α2-adrenergic blocker: 1 mg/kg iv). Results: Stimulation of select mediastinal nerves sites consistently elicited atrial tachyarrhythmias. Combined α-adrenergic blockade eliminated atrial tachydysrythmia induction in every animal. Naftopidil or yohimbine alone mitigated atrial arrhythmia induction. Conclusions: Excessive activation of select intrinsic cardiac neural components induces atrial arrhythmia. This neurally based arrhythmic substrate can be suppressed by α-adrenoceptor blockade. Treatment targeting select neural elements with ICN has potential therapeutic benefits for atrial arrhythmias management. Supported by the CIHR, the Québec Heart & Stroke Foundation and the NIH.
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