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Objectives To develop a cellular model of hypoxia in isolated guinea pig ventricular cardiocytes, and to determine the direct relation between hypoxia-induced action potential shortening and opening of ATP sensitive potassium channels.Methods Myocytes were isolated from ventricles of adult guinea pig hearts, the patch clamp technique in the whole cell configuration was used to study ionic current, and experiments were performed in an experimental chamber that allowed the cells to be exposed to a sufficiently low O2 pressure. Results Hypoxia abbreviated action potential (384±65 ms to 188±46 ms, P<0.05, n=10). After 5-20minutes of hypoxia, the time independent outward current developed gradually, which had a linear current-voltage relation between -100 mV and +100 mV, and reversed at the resting potential of cell. The hypoxia-induced time independent outward current which can be blocked by 5 μmol/L glibenclamide and was inhibited by the diffusion of 3 mmol/L ATP into the pipettes. However, ICa showed a markedly run-down during hypoxia and did not recover after recoxygenation.Conclusions Hypoxia-induced outward current is carried by K+ probably through KATP channels, opens as cytosolic ATP concentration, and falls below a critical threshold. Opening of KATP channels is directly related to hypoxia-induced action potential shortening.