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A A Vinokurov

Publications and source records attributed to A A Vinokurov.

At least 19 recordsLinked to original sources
PubMed2004

[Some mechanisms of adenosine protective effect in the "calcium paradox"].

A possibility of preventing the "calcium paradox" with the aid of adenosine was studied as well as some mechanisms of adenosine effect upon the heart in case of the "calcium paradox". Adenosine was found to suppress release of amino acids from the heart in perfusion with calcium-free medium, to efficiently prevent disorders in the energy-dependent functions of mitochondrion and myoglobin release from the heart in reperfusion with Ca2+ -containing solution. Adenosine was also found to increase 2-10-fold lactate release from the heart. Adenosine seems to be able to activate glycolysis. Iodine acetate was shown to completely suppress the adenosine ability to decrease amino acid release from the heart perfused with calcium-free medium. Under conditions of iodine acetate blocking of glycolysis was found to possess no protective properties against cytolysis in the "calcium paradox". The heart mitochondria isolated in the end of the experiment revealed low values of free or phosphorylating respiration and complete dissociation of oxidation. Also a protective effect of adenosine in inhibition of Na+, K+ -ATPhase with Strophantinum, was studied.

Adenosine↗
PubMed2004

[Dependence of myocardial contracture on energy resources during the calcium paradox].

Perfusion of the rat isolated hearts with calcium-free and calcium containing solution revealed a complex and deep myocardial damage called the calcium paradox. The reperfusion of the rat heart with calcium rich media resulted in myoglobin loss from the heart, significant decreasing of ATP and phosphocreatine level, complete uncoupling of respiration and phosphorylation in mitochondria, occurrence of myocardial contracture. Decreasing of sodium level to 30 mM--80 mM in calcium free media exacerbates the heart damage due to the calcium paradox with absence of contracture. Addition of phosphocreatine (1 mM, 5 mM, 10 mM) evoked some restoration of ATP contents in the tissue with appearance of significant contracture. Phosphocreatine exacerbated the loss of myoglobin from the heart subjected to the calcium paradox. A discrepancy between myocardial contracture and degree of cellular damage has been observed during the calcium paradox.

Animals↗
PubMed2003

[Dependence of myocardium injury on extracellular K+ concentration during calcium paradox].

It is well-known that the first stage of the calcium paradox involves decreasing of Na+ gradient. The decreased sodium gradient is a cause of activation of the Na(+)-Ca+ exchange and formation of cardiac injury during the calcium repletion. Potassium ions are natural extracellular activators of Na(+)-pump. It has been shown that heart perfusion by Ca(2+)-free medium evoked extrusion from cells of hydrophilic amino acids whose transport-depends on sodium gradient. The heart reperdusion with Ca(2+)-containing agent leads to myofibrillar contracture and extensive myoglobin release. The simultaneous events are: elevation in tissue water contents, decreasing of intracellular concentration of adeninnucleotides, uncoupling of oxidation and phosphorylation in mitochondria. The decreasing of K+ level to 0.5 mM exacerbates myocardial damage during the calcium paradox, despite absence of myocardial contracture. The elevation of K+ (to 10 mM or 20 mM) attenuated the calcium paradox development in the heart. The elevated K+ concentration protected isolated heart from extensive myoglobin release, development of myocardial contracture. The high K+ concentrations alleviate mitochondrial damage and elevate contents of adeninnucleotide in the tissue. The positive effect of the elevated K+ concentration can be completely blocked by strophanthine, the selective Na+, K(+)-pumb blocker.

Adenine Nucleotides↗
PubMed2001

[Mechanisms of action of hypersodium medium on contractile activity of isolated rat heart].

Despite the high efficiency of elevated concentrations of sodium ions during myocardial ischemia and calcium paradox, the molecular mechanism of action of hypersodium media on heart contractions remains unknown. The purpose of the investigation was to study mechanisms by which raised concentrations of sodium ions alter cardiac contractility. Subsequent to initially developed reduced pressure in the left ventricle, elevated concentrations of sodium ions (200 mM instead of 140 mM NaCl, 3 mM KCl) produced an increased force of contractions of about 50%. The first stage of decrease in developed pressure did not relate to elevated tonicity of extracellular ionic millieu because lithium chloride (60 mM) did not produce the same effect. This action of elevated concentrations of sodium ions has been shown to be independent of blockers of ion-transporting systems (caffeine, verapamile, ethmozine, HMA or lidocaine). Raising the contractions by elevating the concentration of sodium ions (second stage) has been shown to be susceptible to sodium channel blockers (6-IA, benzamil, of phenamil) and to caffeine. Decreasing of potassium concentration (from 3 mM to 1-2 mM amplified, and increasing of K+ level (from 3 mM to 6 mM) attenuated the positive inotropic action of the elevated concentration of sodium ions. The positive inotropic effect due to elevated concentrations of sodium ions remains even after heart arrest by high concentrations of verapamile (2 mcM). Lithium chloride (60 mM) failed to elevate left ventricle developed pressure which was raised by elevated concentrations of sodium ions. These data suggest that the elevated concentration of sodium ions could effect Na+/Ca2+ exchange and provoke Ca2+ release from sarcoplasmic reticulum by changing the sodium gradient and resulting in Ca2+ entry via Na+/Ca2+ exchange. These observations are consistent with the hypothesis of Leblanc N., Hume J.R. (1990) regarding sodium-induced calcium ion release from sarcoplasmic reticulum.

Animals↗
PubMed2000

[Effect of sarcolemmal ion-transporting system blockers on the intensity of heart damage during "calcium paradox"].

The aim of present study was to investigate a role of different anions in calcium paradox development. It is accepted point of view that development of calcium paradox is depend on cation composition and activity of Na/Ca exchange. However, role of anion composition remain unknown. It is not studied role of some aniontransporting systems in development of calcium paradox. Experiments were carried out on isolated Langendorff perfused rat hearts. Hearts were perfused with calcium-containing solution for 15 minutes, calcium-free medium for 10 minutes and reperfused by initial calcium-containing solution with [Ca2+ = 2 mM]. Release of myoglobin was used as a marker of membrane damage. It has been shown that addition of 5-20 mM HCO3 exacerbated calcium paradox of the heart, elevated myoglobin release from 4.92 +/- 0.57 mcg/g dry weight to 11.3 +/- 1.6 mcg/g dry weight. An inhibitor of HCO3/Cl exchange, 10 mcM L-644,711 depressed elevation of myoglobin release to 4.8 +/- 1.05 mcg/g dry weight. An inhibitor of Cl- channels, 5 mcM DIOA caused raising of myoglobin loss to 7.3 +/- 0.8 mcg/g dry weight during calcium paradox. These data show dependence of calcium paradox on anion composition. A possible reason for exacerbation of calcium paradox by HCO3- rich medium could be consistence of HCO3/Cl and Na/Ca exchange. The results discover new perspectives in myocardial protection of calcium overload.

Animals↗
PubMed1999

[Effect of the ion composition of the calcium-free medium and cardiomyocyte damage during "calcium paradox" in rats].

The findings reveal that the degree of myocardial damage in the "calcium paradox" does not depend on the contracture strength, that the contracture attenuation due to a decreased concentration in the Ca-free medium is not equal to the cardiocytes protection as compared with other means. Mg2+ and the studied means of myocardial protection seem to play a major role in assessment of the "calcium paradox" development and explain the difference in results of the hyposodium medium effects in the "calcium paradox".

Animals↗
PubMed1999

[Dependence of myocardial damage on the anion composition and osmotic pressure in the extracellular fluid during "calcium paradox" in rats].

The data obtained reveal that elevation of extracellular osmolarity with sucrose during reintroduction of Ca-containing medium after 10 minutes of Ca2+ removal prevents loss of haemoglobin in a concentration-dependent mode. Reducing the extracellular osmolarity of the reperfusion medium by means of decreasing the concentration of sodium chloride and calcium chloride exacerbates the loss of haemoglobin from the cardiomyocytes. There is a close correlation between the water contents in tissues and the loss of haemoglobin during the "calcium paradox". The findings suggest dependence of the heart damage during the "calcium paradox" on anionic composition of extracellular space and activity of anionic transporters.

Animals↗
PubMed1999

[The importance of the ion-transport systems of the sarcolemma and sarcoplasmic reticulum in changing rat cardiac contractile function under a hypersodium medium].

Following a reduced pressure in the left ventricle, elevated concentrations of sodium ions enhanced by half the contraction force of the rat isolated heart. This effect was shown to be independent of the Na-channels blockers or Na/H exchange of caffeine but quite susceptible to sodium channel blockers, caffeine, and the blocking agent for Na-Ca exchange Ni2+. A decrease in potassium concentration amplified, and elevation of K+ level attenuated the positive inotropic effect of the elevated concentration of sodium ions. The effect was preserved even after heart arrest induced by verapamil. The findings suggest that elevated concentration of sodium ions may affect the Na+/Ca2+ exchange and provoke Ca2+ release from sarcoplasmic reticulum by means of changing the sodium gradient. These data corroborate the Leblanc and Hume hypothesis of the sodium-induced calcium ions release from sarcoplasmic reticulum.

Amiloride↗
PubMed1999

[Dependence of the protective effect of the elevated sodium level on the type of oxidative substrate in the isolated heart during "calcium paradox"].

Isolated guinea pig heart were perfused with the Tyrode solution followed in 15 min. by a 10-min. Ca(2+)-free solution with subsequent return to the normal Ca(2+)-containing Tyrode solution. Sarcolemma damage was measured by myoglobin release. The perfusion resulted in damage of the myocardium cells. The data obtained show that elevation of the extracellular pressure during reperfusion with the Ca(2+)-containing medium is more important than the absolute value of the osmotic pressure.

Animals↗
PubMed1998

[Dissociation between the development of myocardial contracture and heart damage in the "calcium paradox"].

The interrelationship between contracture development and heart damage during the calcium paradox under different sodium concentration in Ca-free media was studied on isolated rat hearts. It had been shown that calcium paradox development accompanied contracture development, intensive membrane disruption and alteration of tissue energy state. We had not found relation between contracture magnitude and degree of myocardial alterations in calcium paradox. Our dates confirm so-called intracellular hypothesis of calcium paradox. The experiments had shown close correlation between transmembrane sodium gradient in Ca-free media and degree of cellular damage and energy state alterations during calcium readmission in solution.

Analysis of Variance↗
PubMed1997

Effect of histidine-containing dipeptides on isolated heart under ischemia/reperfusion.

The protective effects of carnosine and related compounds on isolated rat heart were studied under experimental ischemia. The ability of carnosine to suppress significantly the development of ischemic reperfusion contracture and to support the restoration of the contractile force during reperfusion were shown. At the same time, a decrease of myoglobin and nucleoside release from myocytes was observed, this indicating a membrane-protecting effect of carnosine. Methylation of carnosine at the N1 or N3 atom of the imidazole ring significantly decreased the protective effect; the substitution of beta-alanine with gamma-aminobutyric acid (resulting in formation of homocarnosine) actually augmented ischemic damage to the heart. Acetylation of carnosine at the beta-amino group amplified the membrane-protecting properties of the molecule, the acetylated derivative of carnosine also showing the ability to induce contractile activity of the ischemic heart. Histidine alone or in combination with beta-alanine and sodium acetate had no effect, while acetylhistidine showed a significant protective effect during reperfusion. The comparison of the effects of natural histidine-containing dipeptides versus synthetic antioxidants indicates that the anti-ischemic effect of carnosine and acetylcarnosine involves antiradical and membrane-protecting mechanisms; nevertheless, the effect cannot be reduced to these mechanisms alone. The observed phenomena of heart muscle protection by acetylated derivatives of carnosine and anserine under ischemia correlates with the preferential localization of these compounds in high quantities in the myocardium.

Animals↗
PubMed1997

[The protective action of adenosine in the development of the "calcium paradox" in the isolated heart].

Calcium repletion (2.0 mM) after 10 min of calcium depletion (pCa = 7) resulted in the loss of myoglobin, decreased contents of ATP and adeninucleotides. Adenosine in concentration 50-1000 mcM depressed the release of myoglobin and prevented depletion of ATP and adenine nucleotides during the "calcium paradox". Theophylline, a non-selective A1-receptors blocker did not alter either "calcium paradox" development or protective effect of adenosine. Dipiridamole, an inhibitor of transmembrane transport of adenosine, protected hearts against the "calcium paradox" depending on the concentration. Dipiridamole (50 mcM) abolished protective effect of high concentrations (100-1000 mcM) of adenosine. The results obtained prove that transmembrane transport of adenosine is more important than its interaction with receptors for its protective effect under the "calcium paradox".

Adenosine↗
PubMed1992

[Metabolism of extracellular phosphocreatine during changes in the ionic composition of the medium in the perfused rat heart].

Perfusion of isolated rat hearts with a phosphocreatine (10(-4) M) containing solution to which strophanthin or KCl had been added up to a concentration of 27 mM as well as Ca2+ depletion decreased phosphocreatine concentration in the perfusate with a simultaneous increase in creatine and phosphocreatine concentrations in the myocardium. Neither high extracellular concentrations of Na+ (200 mM), nor phosphocreatine increased creatine and phosphocreatine levels in the myocardium. The effect of high sodium perfusion media was completely reversed by strophanthin. Phosphocreatine decreased the lactate content in the perfusate. Strophanthin or potassium chloride enhanced the effect of phosphocreatine on the lactate release. Conversely, creatine augmented the lactate content in the perfusate. A high specificity of the phosphocreatine effect on the myocardium independently of the ionic composition of the perfusate was postulated. A mechanism of protective effects of phosphocreatine and high sodium perfusion media on "calcium paradox" is proposed.

Animals↗
PubMed1992

[Significance of extracellular concentration of sodium ions in the protective effect during the "calcium paradox"].

Increasing of extracellular sodium concentration up to 200 mM diminishes heart damage under "calcium paradox". Phosphocreatine (10(-4) M) potentiates the effect of high sodium perfusion media; in this case myoglobin release from the myocardium is minimal (5-9% of control). An the same time, ATP and phosphocreatine concentrations and oxidation to phosphorylation coupling in mitochondria remain at a sufficiently high level. Elevation of osmotic pressure by the effect of 120 mM sucrose enhances heart damage under "calcium paradox" both in the presence and absence of phosphocreatine. The protective effects of superhigh (200 mM) sodium concentrations and phosphocreatine are completely reversed by strophanthin or decreasing K+ concentration down to 0.5 mM.

Adenosine Triphosphate↗
PubMedDate not supplied

[The role of ion transport system of sarcolemma in amino acid loss during myocardial perfusion with calcium-free medium and myocardium injury during "calcium paradox"].

The loss of myocardial amino acids is known to depend on sodium gradient across sarcolemma. This is regulated by changes of cellular volume as well. It is suggested that loss of amino acids can be regulated by blocking of anion-transporting systems during Ca-free perfusion. It have been found that calcium depletion from extracellular medium exacerbates release of amino acids two- four fold. Sodium lowering (from 140 mM to 30 mM) accelerates and sodium elevation (from 140 mM to 200 mM) attenuates loss of taurine, glutamine, glycine, glutamate, aspartate, alanine and asparagine, but does not hydrophobic amino acids. Inhibition of CI- channels by IAA94 or K-Cl cotransport with DIOA increases the loss of taurine, glutamine, glycine, glutamate, aspartate, alanine and asparagine during Ca-free perfusion. The release of amino acids during Ca-free perfusion is negatively correlated with recovery of oxidative phosphorylation during the second phase the calcium paradox-Ca-readmission.

Amino Acids↗