Ventricular arrhythmias following myocardial infarction may originate from subendocardial Purkinje fibres in the infarcted area. The role of potassium and sodium-calcium exchange currents on action potential duration was therefore investigated in Purkinje fibres surviving infarction and in normal Purkinje fibres. Barium was used to reduce potassium conductance and replacement of sodium chloride by lithium chloride was used to reduce the sodium-calcium exchange current. Barium (1 x 10(-5) to 3 x 10(-5) M) produced a concentration dependent lengthening of action potential duration in normal Purkinje fibres but these concentrations had no effect in Purkinje fibres surviving infarction. The resting membrane potential, activation voltage, amplitude and Vmax were decreased in Purkinje fibres surviving infarction and in barium treated fibres v normal Purkinje fibres. These results show that action potential characteristics of barium treated normal Purkinje fibres closely resemble those seen in Purkinje fibres surviving infarction. A similar reduction of action potential duration was seen in normal Purkinje fibres, fibres surviving infarction and barium treated fibres when the sodium "window" current was decreased by lignocaine. Without any effect on the Vmax, the replacement of sodium chloride by lithium chloride resulted in a similar effect on the action potential duration in normal Purkinje fibres and fibres surviving infarction. The results show that the longer action potential duration found in Purkinje fibres surviving infarction can be explained by a decrease of the potassium conductance and not by an increase of the sodium "window" current or the sodium-calcium exchange current.