title: [Response of experimental ventricular tachycardia to class I anti-arrhythmia agents].
abstract: Active ventricular arrhythmias were provoked in damaged dog myocardium to study their response to some antiarrhythmic agents of Vaughan-Williams' class I. Dogs anesthetized with intravenous sodium pentobarbital (30 mg/Kg) were intubated and submitted to artificial ventilation using a Palmer pump. An infarction was produced near the apex of the left ventricle by intramural injection of 1-1.5 ml of phenol, and 30 to 60 min later, minute crystals of aconitine were introduced into the periphery of the infarcted area. Once ventricular tachycardia appeared and became stable, corresponding records were obtained and the antiarrhythmic agent to be studied was administered through the superior vena cava over a period of 5 to 15 min. Electrocardiographic tracings were registered at constant intervals in order to detect the recovery and duration of sinus rhythm. The reappearance of arrhythmia was always required in order to consider the action of the medication administered positive. High doses of lidocaine (6 mg/Kg) reestablished transient sinus rhythm in 23% of 35 treated dogs. Fifteen mg/Kg of mexiletine reestablished it in 45% of 22 animals and 2.5 mg/Kg of propafenone restored it in 39% of 18 animals receiving this drug. The positive effect of these antiarrhythmic agents of groups I B and I C consisted essentially in controlling no-rapid tachycardias with the "wave jumping" phenomenon and fusion beats, which may be due to activity of ectopic foci. Very rapid ventricular tachycardia with "wave jumping" generally did not respond to the antiarrhythmic agents tested. These tachycardias may be maintained by reentry or by the intervention of calcium-dependent potentials. Rapid ventricular tachycardias without extensive "wave jumping" also occurred. These were never controlled by the group I B antiarrhythmic agents, although they were sometimes suppressed with propafenone. These tachycardias probably originated near the intraseptal barrier. In few animals, amiodarone of class III was employed with a marked hypotensive effect.
authors.affiliation: Departamento de Farmacología, Instituto Nacional de Cardiología, Ignacio Chávez, México.
authors.forename: A
authors.initials: A
authors.lastname: de Micheli
authors.forename: G A
authors.initials: GA
authors.lastname: Medrano
mesh_terms: D000638:Amiodarone / Q000627:therapeutic use; D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use*; D004285:Dogs; D004562:Electrocardiography; D006352:Heart Ventricles; D008012:Lidocaine / Q000627:therapeutic use; D008801:Mexiletine / Q000627:therapeutic use; D011405:Propafenone / Q000627:therapeutic use; D013610:Tachycardia / Q000175:diagnosis / Q000188:drug therapy*
chemical_list: D000889:Anti-Arrhythmia Agents; D008801:Mexiletine; D011405:Propafenone; D008012:Lidocaine; D000638:Amiodarone
vernacular_title: Respuesta de taquicardias ventriculares experimentales a antiarritmicos de la clase I.