Adenosine receptors and PKC activations are needed to IPoC protection, but not KATP channels. (A) Since some of the drugs were dissolved in dimetilsophoxide (DMSO) also postconditioning was performed under this condition (IPoCd). Arrhythmias’ severity during reperfusion was reduced by IPoCd and all co-administered treatments abrogated protection except glibenclamide (IPoC + GLI). (B) Adenosine receptors inhibitors and glibenclamide, but not chelerythrine, prevented action potential shortening induced by IPoCd. In the inset, the action potentials were artificially aligned to 0 phase for better contrast of APD. The arrow indicates a delayed afterdepolarization. (C) Adenosine receptors blockade and glibenclamide prevented the transient shortening induced by IPoCd during the first 3 min of reperfusion, but CHE did not affect APD shortening.