In experiments on the anaesthetized dogs with modeling of experimental ischemia (90 min) and reperfusion (180 min) it was investigated the changes of biochemical processes in the different areas of heart ( intact, risk and necrotic zone) during intragastric introduction of medicinal form (tablets) of flocalin ( the fluorine-containing opener of ATP-sensitive potassium channels) in a dose 2,2 mg/kg. The data analysis allowed to define a few possible cardioprotective mechanisms of flocalin action at ischemia-reperfusion conditions: the preservation of sufficient levels of de novo (by cNOS) NO synthesis, an inhi­bition of de novo (by iNOS) and salvage (by NADH-depen-dent nitratreductase) NO synthesis, an inhibition of L-arginine degradation by arginase, an inhibition of oxidizing metabolism due to limitation of ROS and RNS generation, inhibition of free arachidonic acid and eicosanoids synthesis, inhibition of AT P and GTP degradations and, possibly, stimulation of pro­tective haem degradation. These changes may prevent forma­tion of toxic peroxynitrite and suggest the possibility of par­ticipating in flocalin–mediated cardioprotective effects of warn­ing a mitochondrial permeability transition pore (MPTP) open­ing and inhibition of apoptosis and/or necrosis of cardiomyo-cytes induced by it.