Experimental arrhythmia elicited by low K perfusion.

Isolated rabbit hearts undergo ventricular depolarization when exposed to 0.5 mM K--Krebs during 30 to 45 min. A ventricular tachyarrhythmia develops when these hearts are allowed to repolarize in 1.5 mM K--Krebs. Ventricular fibrillation usually follows. These arrhythmias do not cease spontaneously. Initially, perfusion with 0.5 mM K hyperpolarized the membrane to -100 +/- 1.2 mV (means +/- SEM), decreased the plateau level, greatly increased the action potential duration, and slowed down intraventricular conduction, despite the level of membrane polarization and a high rate of rise of the upstroke. After a delay of 15 to 30 min, a progressive depolarization occurred and a stable potential level of -61 +/- 1.9 mV was reached. The arrhythmia elicited by perfusion with 1.5 mM K was of ventricular origin but did not appear when the previous exposure to 0.5 mM K was reduced to 10 min. Addition of verapamil (1.0 microM) to the 1.5 mM K medium did not prevent the early appearance of the arrhythmia, but restored driven electrical activity after variable delays despite the persistence of alterations in the action potential configuration. Verapamil also abolished the slow depolarizing phase of the upstroke. It is proposed that the abnormal electrical activity arose in a partly depolarized Purkinje network and it may have been triggered by the electrical nonhomogeneity created by the repolarization of ventricular cells in an extracellular K+ concentration of 1.5 mM.