Mechanisms for Vagal Modulation of Ventricular Repolarization and of Coronary Occlusion-Induced Lethal Arrhythmias in Cats

Our goal was to better understand the mechanisms underlying muscarinic receptor actions on the ventricle in vivo. Therefore, we studied the effects of vagal stimulation on ventricular repolarization and of vagal tone on lethal arrhythmias induced by 30 minutes of left anterior descending coronary ar...

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Bibliographic Details
Published in:Circulation research 1994-10, Vol.75 (4), p.722-732
Main Authors: Rosenshtraukh, Leonid, Danilo, Peter, Anyukhovsky, Evgeny P, Steinberg, Susan F, Rybin, Vitalyi, Brittain-Valenti, Kimberly, Molina-Viamonte, Victor, Rosen, Michael R
Format: Article
Language:English
Subjects:
Acetylcholine - pharmacology
Animals
Arrhythmias, Cardiac - etiology
Arrhythmias, Cardiac - physiopathology
Atropine - pharmacology
Cardiac Pacing, Artificial
Cats
Coronary Disease - complications
Electrocardiography
Electrophysiology
GTP-Binding Proteins - analysis
Heart Ventricles - drug effects
Heart Ventricles - physiopathology
In Vitro Techniques
Pertussis Toxin
Propranolol - pharmacology
Vagus Nerve - physiology
Ventricular Fibrillation - etiology
Ventricular Fibrillation - physiopathology
Virulence Factors, Bordetella - pharmacology
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Summary:Our goal was to better understand the mechanisms underlying muscarinic receptor actions on the ventricle in vivo. Therefore, we studied the effects of vagal stimulation on ventricular repolarization and of vagal tone on lethal arrhythmias induced by 30 minutes of left anterior descending coronary artery ligation in anesthetized cats. Experimental groups included normal control cats subjected only to coronary ligation and cats pretreated with atropine, pertussis toxin (PTX), or propranolol. All cats received bilateral cervical vagal stimulation (Vstim) at 1, 3, and 5 Hz for 1 minute at 10-minute intervals. Before coronary ligation, Vstim slowed sinus rate, prolonged the PR interval, and lowered blood pressure. Most important from the point of view of electrophysiological function was a vagally induced acceleration of ventricular repolarization in paced and unpaced hearts, which could be explained by the effects of acetylcholine (ie, shortening the subepicardial muscle action potentials). The effect on repolarization was blocked by atropine or PTX but not by propranolol. The extent of sinus slowing and acceleration of repolarization was directly related to the level of functional PTX-sensitive G protein (P
ISSN:0009-7330
1524-4571
DOI:10.1161/01.res.75.4.722