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AIM: To study the effects of hepatic ischemia/reperfusion (I/R) injury on store-operated calcium channel (SOC) currents (Isoc) in freshly isolated rat Kupffer cells, and the effects of Ca2+ channel blockers,2-aminoethoxydiphenyl borate (2-APB), SK&F96365,econazole and miconazole, on Isoc in isolated rat Kupffer cells after hepatic I/R injury.METHODS: The model of rat hepatic I/R injury was established. Whole-cell patch-clamp techniques were performed to investigate the effects of 2-APB,SK&F96365, econazole and miconazole on Isoc in isolated rat Kupffer cells after hepatic I/R injury.RESULTS: I/R injury significantly increased Isoc from-80.4 ± 25.2pA to -159.5 ± 34.5pA (bP ＜ 0.01, n = 30).2-APB (20, 40, 60, 80, 100 μmol/L), SK&F96365 (5, 10,20, 40, 50 μmol/L), econazole (0.1, 0.3, 1, 3, 10 μmol/L)and miconazole (0.1, 0.3, 1, 3, 10 μmol/L) inhibited Isoc in a concentration-dependent manner with IC50 of 37.41 μmol/L (n = 8), 5.89 μmol/L (n = 11), 0.21 μmol/L (n = 13), and 0.28 μmol/L (n = 10). The peak value of Isoc in the Ⅰ-Ⅴ relationship was decreased by the blockers in different concentrations, but the reverse potential of Isoc was not transformed.CONCLUSION: SOC is the main channel for the influx of Ca2+ during hepatic I/R injuries. Calcium channel blockers, 2-APB, SK&F96365, econazole and miconazole,have obviously protective effects on I/R injury, probably by inhibiting Isoc in Kupffer cells and preventing the activation of Kupffer cells.