Ventricular tachycardia in an isolated guinea pig ventricular free wall model of ischemia and reperfusion.

Electrical activity from endo- and epicardium was recorded from isolated segments of right ventricular free walls of guinea pigs using standard differential microelectrode techniques and a high-gain electrocardiogram (ECG). Stimulation was applied to the endocardium. Tissues were exposed to ischemic conditions for 10 min and then were reperfused with "normal" Tyrode's solution. Early premature beats or rapid ventricular tachycardia (VT) occurred in 36% of hearts during "ischemia" and 79% of hearts on reperfusion. Endocardial activation was not significantly slowed by ischemic conditions or reperfusion. However, transmural conduction times increased, and muscle action potential durations decreased during ischemic conditions and early reperfusion. Rapid VT began with alternating activation of endo- and epicardium, and continuous low-voltage ECG activity bridging diastole. Activation of epicardium was essential for occurrence of early premature beats and rapid VT. Hyperkalemia during ischemia promoted arrhythmias during "ischemia," but not during reperfusion. Oscillatory afterpotentials (OAP) also occurred during reperfusion (36%), but not during "ischemia". Our study provides an isolated tissue model that reproducibly generates tachycardias, and that permits study of ischemia and reperfusion-induced transmembrane activity and defects in transmural conduction.