Abstract
A model was developed to study ventricular automaticity and reentry in the heart of open chest dogs during myocardlal ischemia. Atrioventricular (A-V) block and the resultant idioventricular rhythm were induced by surgical destruction of the His bundle, and acute myocardial ischemia was produced by ligation of the left anterior descending coronary artery. The ventricle was paced by basic stimuli, and one or two premature beats were introduced at various coupling Intervals after the 10th basic beat. Two different types of response to these premature beats could be observed: (1) rapidly repetitive beats or fibrillation due to reentry after early premature beats, and (2) the appearance of escape beats from idioventricular automatic fibers after late premature beats. With this model of ventricular reentry and automaticity, the effect of procainamide (group I antiarrhythmic agent) was studied in 12 dogs, and that of lidocaine (group II) in 13 dogs. Both procainamide and lidocaine were effective in decreasing automaticity since they significantly increased postextrasystolic escape intervals of idloventricular beats. Although procainamide failed to abolish the reentrant beats induced by early premature beats in all 12 dogs, lidocaine abolished these beats in 10 of 13 dogs. The results indicate that lidocaine is much more effective than procainamide in preventing ventricular reentrant activity induced by early premature beats.
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