Tl+-ions: effects on the automaticity of sinoatrial tissue and dV/dtmax and iK2 of cardiac Purkinje fibres.

The disrhythmic effects of thallium were investigated in various cardiac tissues to determine the primary site of intoxication with respect to ensuing arrhythmias. In isolated cardiac tissue Lameijer and van Zwieten [1] had contended that arrhythmias arise from the sinus node after thallium poisoning. To test this hypothesis we administered concentrations of Tl+ between 10(-7) and 10(-4) M to guinea pig sinoatrial preparations, to guinea pig papillary muscles and to sheep cardiac Purkinje fibres. In sinoartial preparations thallium provoked increases and decreases of spontaneous beat frequency which were not linked to corresponding changes in contractile force. In conductive tissue, Purkinje fibres, the inactivation kinetics of the fast sodium current and the pacemaker current iK2 were investigated by voltage clamp experiments. Here, thallium was seen to be essentially without toxic effects which could account for arrhythmias. In ventricular muscle actions potentials and contractile force were recorded simultaneously. Here again, ventricular arrhythmias are not to be expected from thallium intoxication in rather high concentrations. The findings support the view that arrhythmogenic effects of thallium are restricted to the sinus node.