AIM: To determine the changes of delayed rectifier K+ currents (Ik) and inward rectifier K+ currents (Ik1) in the ventricular myocytes of guinea pigs during the gradual apoptotic process by the chronic oxidant stress treatment. METHODS: H2O250 μmol/L (24 h) was used for inducing apoptosis in the cardiomyocytes culture of neonatal rats and to treat the isolated ventricular myocytes of adult guinea pigs in vitro for 24 h. Apoptosis was evaluated by TUNEL methods and voltage-dependent K+ currents were recorded by patch-clamp techniques. RESULTS: H2O2 50 μmol/L (24 h)induced cell apoptosis in the cardiomyocytes culture of neonatal rats. This concentration was used to treat the isolated ventricular myocytes of adult guinea pigs in vitro for 24 h and the voltage-dependent K+ currents densities (Ik, Ik1) were down-regulated. The densities of the delayed rectifier K+ currents (Ik) in 50 μmol/L H2O2 group were 2.52±0.57 pA/pF vs 5.73±1.84 pA/pF in the control group at +50 mV (n=8, P<0.01). The densities of the inward rectifier K+ currents (Ik1) in 50 μmol/L H2O2 group were -13.9± 2.70 pA/pF, 2.52±0.57 pA/pF vs -59.7±11.9 pA/pF, 5.73±1.84 pA/pF in the control group at -120 mV (n=8, P< 0.01) and -40 mV (n=8, P<0.05), respectively. The extent of inward rectifier property of Ik1 was weakened by 50 μmol/L H2O2treatment. CONCLUSION: The densities of Ik, Ik1 in the cardiomyocytes of guinea pigs were down- regulated and the inward rectifier property of Ik1 was weakened during the gradual apoptotic process after 50 μmol/L H2O2 treatment for 24 h. AIM: To determine the changes of delayed rectifier K + currents (Ik) and inward rectifier K + currents (Ik1) in the ventricular myocytes of guinea pigs during the gradual apoptotic process by the chronic oxidant stress treatment. METHODS: H2O250 μmol / L (24 h ) was used for inducing apoptosis in the cardiomyocytes culture of neonatal rats and to treat the isolated ventricular myocytes of adult guinea pigs in vitro for 24 h. Apoptosis was evaluated by TUNEL methods and voltage-dependent K + currents were recorded by patch-clamp techniques. RESULTS: H2O2 50 μmol / L (24 h) induced cell apoptosis in the cardiomyocytes culture of neonatal rats. This concentration was used to treat the isolated ventricular myocytes of adult guinea pigs in vitro for 24 h and the voltage-dependent K + currents densities The densities of the delayed rectifier K + currents (Ik) in 50 μmol / L H2O2 group were 2.52 ± 0.57 pA / pF vs 5.73 ± 1.84 pA / pF in the control group at +50 mV ( n = 8, P <0.01). The densities of the inward rectifier K + currents (Ik1) in 50 μmol / L H2O2 group were -13.9 ± 2.70 pA / pF, 2.52 ± 0.57 pA / pF vs -59.7 ± 11.9 pA / pF, 5.73 ± 1.84 pA / pF in the control group at -120 mV (n = 8, P <0.01) and -40 mV (n = 8, P <0.05), respectively. The extent of inward rectifier property of Ik1 was weakened by 50 μmol / L H2O2treatment. CONCLUSION: The densities of Ik, Ik1 in the cardiomyocytes of guinea pigs were down-regulated and the inward rectifier property of Ik1 was weakened during the gradual apoptotic process after 50 μmol / L H2O2 treatment for 24 h.