Inhibitory effect of anoxia on reperfusion- and digitalis-induced ventricular tachyarrhythmias.
In the isolated rat heart, anoxia or ischemia do not induce important ventricular tachyarrhythmias (VTAs). During the 1st min of reperfusion, VTAs are frequent. The frequency and severity of VTAs during reperfusion depend on the duration and the extent of the myocardial damage. Anoxia abolishes reperfusion-induced VTAs as did verapamil (2.5 X 10(-6) M). In isolated guinea pig hearts, beta-methyldigoxin (1.27 X 10(-6) M) provokes VTAs that are progressively increasing in severity. After 26 min of perfusion with an oxygenated beta-methyldigoxin-containing medium, all isolated guinea pig hearts develop ventricular fibrillation. By changing the abnormal rapid ventricular rhythms into progressively slower irregular idioventricular rhythm, anoxia counteracts all types of VTAs exhibited by the intoxicated guinea pig hearts. In conclusion, two conditions seem to be necessary for the development of VTAs during the reperfusion: 1) a sufficient degree of myocardial damage provoked by the preceding ischemic perfusion, and 2) the presence of oxygen during the reperfusion.
D000818:Animals; D003327:Coronary Disease / Q000503:physiopathology*; D006168:Guinea Pigs; D006352:Heart Ventricles; D000860:Hypoxia / Q000503:physiopathology*; D008297:Male; D008520:Medigoxin / Q000494:pharmacology; D010100:Oxygen / Q000502:physiology; D010477:Perfusion; D051381:Rats; D013564:Sympathetic Nervous System / Q000503:physiopathology; D013610:Tachycardia / Q000503:physiopathology*; D014700:Verapamil / Q000494:pharmacology
D014700:Verapamil; D008520:Medigoxin; D010100:Oxygen