Inhibitory effect of anoxia on reperfusion- and digitalis-induced ventricular tachyarrhythmias

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Abstract
In the isolated rat heart, anoxia or ischemia did not induce important ventricular tachyarrhythmias (VTA). During the 1st min of reperfusion, VTA were frequent. The frequency and severity of VTA during reperfusion depended on the duration and extent of myocardial damage. Anoxia abolished reperfusion-induced VTA as did verapamil (2.5 .times. 10-6 M). In isolated guinea pig hearts, .beta.-methyldigoxin (1.27 .times. 10-6 M) provoked VTA that were progressively increasing in severity. After 26 min of perfusion with an oxygenated .beta.-methyldigoxin-containing medium, all isolated guinea pig hearts developed ventricular fibrillation. By changing the abnormal rapid ventricular rhythms into progressively slower irregular idioventricular rhythm, anoxia counteracted all types of VTA exhibited by the intoxicated guinea pig hearts. Two conditions were necessary for the development of VTA during reperfusion: a sufficient degree of myocardial damage provoked by the preceding ischemic perfusion and the presence of O2 during the reperfusion.