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Computer simulations have been used to study the mechanisms of postrepolarization refractoriness in cardiac cells under ischemic conditions at the cellular level. The ten Tusscher model of the cardiac action potential has been used with the formulation of the ATP-sensitive K+ current by Ferrero et al being adopted. Cells were subjected to hyperkalemia, hypoxic and acidic conditions. The results show that the three components of ischemia decrease the action potential duration (APD) as well as the conduction velocity, while effective refractory period (ERP) depicts a non-monotonic behavior. Under hyperkalemic conditions, no supernormal conduction is observed near physiologic values, and conduction relies on ICa(L) for [K+]o > 11 mmol/L. Under hypoxic conditions the trend observed in hyperkalemia are maintained but conduction blocking is obtained at a [K+]o concentration of 10 mmol/L. This condition minimally affects the conduction velocity of the hyperkalemic tissue. Acidosis gradually increases the difference between ERP and APD for reductions above the 60%, with conduction blocking occuring at 90%.