By using two microelectrode voltage clamp technique, the effects of "ischemia" and lysophosphatidylcholine (LPC), a main toxic metabolite in acute ischemic myocardium, on pacemaker current I(f) were examined in sheep cardiac Purkinje fibers. After perfusion with ischemia-like solution for 15, 30 and 60 min, the amplitude of I(f) current was decreased at all membrane potential levels between -60 mV (-) -120 mV (n = 5, P < 0.05), both the activation time and half activation time reaching a steady state value were prolongated (n = 5, P < 0.05), with a result of shifting activation curve of I(f) to a more hyperpolarizing level. In normal Tyrode solution, the amplitudes of I(f) at all measured potential levels were decreased significantly by LPC 2 x 10(-5) mol/L (n = 10, P < 0.05); the steady-state activation curve of I(f) was shifted to a more hyperpolarizing level but the activation time and half activation time to a steady-state value were not changed. When 2 x 10(-5) mol/L LPC was added to the solution after 30 min "ischemia", the amplitude of I(f) decreased significantly at all measured membrane potentials and further more for another 15 min (n = 10, P < 0.05). This suggests that ischemic metabolite LPC may have an inhibitory effect on the normal pacemaker activity of ventricle. Ischemic-like condition could aggravate the suppression of LPC without inducing abnormal strengthening of normal automatic rhythmic activity that might lead to ventricular tachyarrhythmia.