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International Journal of Physiology and Pathophysiology
SJR: 0.116

ISSN Imprimir: 2155-014X
ISSN En Línea: 2155-0158

Archives: Volume 1, 2010 to Volume 9, 2018

International Journal of Physiology and Pathophysiology

DOI: 10.1615/IntJPhysPathophys.v3.i3.60
pages 253-267

Changes in Myocardium Metabolism in Ischemia-Reperfusion and Activation of ATP-Sensitive Potassium Channels

Ruslan B. Strutynskyi
Bogomoletz Institute of Physiology of the National Academy of Sciences of Ukraine, Kyiv
Anatoliy V. Kotsuruba
Bogomolets Institute of Physiology, National Academy of Sciences of Ukraine, Kyiv, Ukraine
Anatolii P. Neshcheret
Bogomolets Institute of Physiology, National Academy of Sciences of Ukraine, Kyiv, Ukraine
Roman A. Rovenets
Bogomoletz Institute of Physiology of the National Academy of Sciences of Ukraine, Kyiv
Olexiy O. Moibenko
Bogomolets Institute of Physiology, National Academy of Sciences of Ukraine, Kyiv, Ukraine

SINOPSIS

In experiments on anaesthetized dogs with simulated experimental ischemia (90 min) and reperfusion (180 min), changes in biochemical parameters were studied in different sites of the heart: intact, risk and necrotic zones after an intraventricular administration of dosage forms (tablets) of flokalin, a fluorine-containing activator of adenosine triphosphate (ATP) -sensitive potassium (KATP) -channels in a dose of 2.2 mg/kg. We examined biochemical indicators that may be defined as possible mechanisms of flokalin action, such as: oxidative metabolism (pools of H2O2, uric acid, diene conjugates, malondialdehyde, eicosanoids LTC4 and TxB2), different ways of NO biosynthesis − oxidative de novo (activity of inducible and constitutive NO-synthase and citrulline pools) and non-oxidizing salvage way (nitrate reductase activity), pools of stable NO metabolites (nitrite and nitrate anions, low and high molecular nitrosothiols), inorganic phosphate and other degradation products of ATP and guanidine triphosphate (GTP), changes in hemoxygenase reaction (pools of bilirubin and iron), non-oxidizing catabolism of L-arginine (arginase activity and pools of urea), and the content of free arachidonic acid. An analysis of the results allowed us to identify several possible cardioprotective mechanisms of flokalin. They involve an inhibition of oxidative metabolism due to limitations of the generation of free oxygen and nitrogen radicals, inhibition of the phospholipid hydrolysis, and thereby formation of free arachidonic acid and pathogenic in myocardial ischemia eicosanoids, inhibition of ATP and GTP degradation, and perhaps stimulation of a protective hemoxygenase response. Inhibition of the inducible de novo and salvage synthesis of nitric oxide, degradation of arginine by arginase and, conversely, maintaining of adequate levels of constitutive de novo nitric oxide synthesis can be considered as an important cardioprotective mechanism. At the same time, preserving the latter on the high level, and above changes in oxidative metabolism that prevent toxic peroxynitrite formation indicate the possibility of flokalin to participate in the cardioprotective effect by preventing mitochondrial permeability transition pore opening and, consequently, inhibiting apoptosis and / or necrosis of cardiomyocytes.


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