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lüll Cervical vagosympathetic and mediastinal nerves activation effects on atrial arrhythmia formation Nadeau R; Cardinal R; Armour JA; Kus T; Richer LP; Vermeulen M; Yin Y; Page PAnadolu Kardiyol Derg 2007[Jul]; 7 Suppl 1 (ä): 34-6In anesthetized dogs both epi-and endocardial atrial activation maps and corresponding isointegral repolarization maps were created before and during right or left mediastinal nerve (RMN and LMN) and cervical vagus nerve (CVN) stimulation. Right mediastinal nerve stimulation typically caused sinus slowing, atrial tachycardia (AT), followed by atrial fibrillation (AF). Activation maps during AT showed epicardial breakthroughs from the right atrial free wall or Bachmann's bundle. Left mediastinal nerve stimulation (LMN) rarely caused sinus slowing and ATs originated mostly from Bachmann's bundle or from the pulmonary vein ostial region. Atrial repolarization changes induced by neural stimulation were measured by integrating the area subtended by 161 epicardial unipolar electrograms. Atrial tachycardia epicardial breakthrough sites were closely associated with the border zone where repolarization changes occurred. Both AT and AF were abolished by I.V. atropine, as were sinus bradycardia and atrial repolarization effects of nerve stimulation. Shortening of latency of onset and duration of AT by I.V. timolol suggest concurrent activation of adrenergic efferent neurons. In conclusion, juxta-cardiac mediastinal nerve stimulation can induce atrial fibrillation from multiple, discrete right and left atrial sites, which correspond to localized repolarization changes. Secondly, sinus bradycardia is not a necessary index of parasympathetic neurally induced atrial fibrillation.|*Body Surface Potential Mapping[MESH]|Animals[MESH]|Atrial Fibrillation/*physiopathology[MESH]|Autonomic Nervous System[MESH]|Disease Models, Animal[MESH]|Dogs[MESH]|Electric Stimulation[MESH]|Ganglia, Parasympathetic/physiopathology[MESH]|Heart Atria/*innervation/physiopathology[MESH]|Vagus Nerve/*physiopathology[MESH] |