The K_ATP channel current (I_KATP) was monitored using the whole cell configuration of the patch clamp technique in single ventricular cardiac myocytes enzymatically isolated from rat hearts. Sodium cyanide, a metabolic inhibitor, was used to mimic cell ischemia. Morphine postconditioning facilitated the further opening of the K_ATP channels. Following initial activation of I_KATP by mimic ischemia, morphine further increased current amplitude by (61.4±13.6)%. K_ATP channels in normal cardiac myocytes were not affected by extracellular applications of morphine alone. Nor-binaltorphimine, a specific κ-opioid receptor antagonist, was unable to abolish the facilitation of morphine postconditioning when administered 5 minutes before morphine. However, naloxone, a non-specific opioid receptor antagonist, and naltrindole, a specific δ-opioid receptor antagonist, can abolish the facilitation of morphine postconditioning. These results indicated that morphine postconditioning facilitate the further opening of the cardiac sarcolemmal K_ATP channels following the channel activation by mimic ischemia. The δ-opioid receptor may be involved in morphine postconditioning.