title: [The changes of metabolism in myocardium at ischemia-reperfusion and activating of the ATP-sensitive potassium channels].
abstract: 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-dependent 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 ATP 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 cardiomyocytes induced by it.
authors.forename: R B
authors.initials: RB
authors.lastname: Strutyns'kyĭ
authors.forename: A V
authors.initials: AV
authors.lastname: Kotsiuruba
authors.forename: O P
authors.initials: OP
authors.lastname: Neshcheret
authors.forename: R A
authors.initials: RA
authors.lastname: Rovenets'
authors.forename: O O
authors.initials: OO
authors.lastname: Moĭbenko
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D016718:Arachidonic Acid / Q000037:antagonists & inhibitors / Q000378:metabolism; D001119:Arginase / Q000037:antagonists & inhibitors / Q000378:metabolism; D001120:Arginine / Q000378:metabolism; D004285:Dogs; D015777:Eicosanoids / Q000037:antagonists & inhibitors / Q000378:metabolism; D006160:Guanosine Triphosphate / Q000378:metabolism; D006418:Heme; D054086:KATP Channels / Q000819:agonists* / Q000378:metabolism; D008929:Mitochondria, Heart / Q000187:drug effects* / Q000378:metabolism; D033681:Mitochondrial Membrane Transport Proteins / Q000037:antagonists & inhibitors / Q000378:metabolism; D000083162:Mitochondrial Permeability Transition Pore; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D050895:Nitrate Reductase (NADH) / Q000378:metabolism; D009569:Nitric Oxide / Q000819:agonists / Q000096:biosynthesis*; D052248:Nitric Oxide Synthase Type I / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D020110:Pinacidil / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000627:therapeutic use; D026361:Reactive Nitrogen Species / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D015427:Reperfusion Injury / Q000188:drug therapy* / Q000378:metabolism
chemical_list: D015777:Eicosanoids; D054086:KATP Channels; D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore; C559719:N-(4-difluoromethoxyphenyl)-N'-pinacolyl-N''-cyanoguanidine; D026361:Reactive Nitrogen Species; D017382:Reactive Oxygen Species; D016718:Arachidonic Acid; D009569:Nitric Oxide; D006418:Heme; D020110:Pinacidil; D006160:Guanosine Triphosphate; D000255:Adenosine Triphosphate; D001120:Arginine; D052248:Nitric Oxide Synthase Type I; D052247:Nitric Oxide Synthase Type II; D050895:Nitrate Reductase (NADH); D001119:Arginase