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Карсанов, Н. В.; Sukoyan, G. V.; Chikobava, E. A.; Karsanov, Z. N.; Yarovaya, E. V.; Tatulashvili, D. R.; Gorelishvili, I. I.

doi:10.1023/a:1021576006103

Cited by 6 publications

(12 citation statements)

References 2 publications

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“…The existence of a close relationship between PPI reflecting changes in free energy of cardiomyocyte and [NAD]/[NADH] redox potential [1][2][3] seems to underlie the pronounced normalizing effect of NAD on the recovery of regulatory interrelations in the AN system. Moreover, under conditions of PPI normalization the decreased content of creatine phosphate can be adaptive and transitory and can result from accelerated utilization of ATP store in the form of creatine phosphate and its effect on anabolic processes.…”

Section: Resultsmentioning

confidence: 99%

“…However, during severe damages and multiple parallel episodes of ischemic and reperfusion stresses, essential recovery of mitochondrial respiratory chain (first of all, cytochrome c) is required. The absence of adequate response of this chain is the major cause of slow rise of creatine phosphate [1][2][3].…”

Section: Resultsmentioning

confidence: 99%

“…The methods for measuring the content of adenine nucleotides (AN), pyridine nucleotides, creatine phosphate, creatine, inorganic phosphates, AN system energy charge, phosphorylation potential PPI and PPII, tension developed by skinned cardiac muscle fibers (SCMF), and statistical methods were described elsewhere [2][3][4]. Poly-(ADP-ribose)-polymerase activity was measured using Amersham Pharmacia Biotech kits [11].…”

Section: Methodsmentioning

confidence: 99%

“…This second group was subdivided into two subgroups: stenosis without treatment (n=10) and stenosis+intravenous injection of NAD (0.5 mg/kg, 2 ml water solution) immediately after 20-min artery clamping (n=8). The details of surgery and hemodynamic recording were described elsewhere [2]. Coronary artery stenosis was modeled as follows: a nylon thread (0.3-0.4 mm) was passed under the artery and attached to a mechanical driver mounted on the myocardial surface, the chest was closed, and a stationary venous catheter was fixed.…”

mentioning

confidence: 99%

“…It was demonstrated that NAD content in the myocardium decreases 10-15 min after coronary occlusion [3], and after 2 h this content was only 25% of the initial value or 70% of normal level [4]. It was hypothesized that NAD degradation play a role in necrotic damage to cells and in transition from reversible to irreversible damage.…”

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confidence: 99%

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Effect of NAD on recovery of adenine nucleotide pool, phosphorylation potential, and stimulation of apoptosis during late period of reperfusion damage to myocardium

Sukoyan

Andriadze

et al. 2005

Bull Exp Biol Med

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The system of energy supply in the myocardium of the left and right ventricles did not recover after short-term circulatory disturbances. ATP synthesis decreased in parallel with activation of poly-(ADP-ribose)-polymerase in the ischemic region of the right ventricle, extra-ischemic region, and in the left ventricle by 5.85, 5.4, and 2.2 times, respectively. Intravenous injection of NAD immediately after blood flow resumption in the subacute period of ischemia-reperfusion damage virtually completely normalized the pool of adenine nucleotides, energy change of the adenine nucleotide system, and phosphorylation potential. Exogenous NAD inhibited activity of poly-(ADP-ribose)-polymerase in the ischemic region of the right ventricle, extra-ischemic region, and in the ischemic region of the left ventricle by 2.4, 2.9, and 1.52 times, respectively. We hypothesize that NAD acts as a regulator of signal mechanism of apoptosis induction during ischemia-reperfusion damages to the myocardium.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Effect of NAD on recovery of adenine nucleotide pool, phosphorylation potential, and stimulation of apoptosis during late period of reperfusion damage to myocardium

Sukoyan

Andriadze

et al. 2005

Bull Exp Biol Med

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Structural and Conformational Changes in Myocardial and Erythrocyte Actin during Cardiac Ischemia

Sukoyan¹,

Berberashvili²,

Tatulashvili³

et al. 2005

Bull Exp Biol Med

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Structural and conformational changes in myocardial and erythrocyte actin during cardiac ischemia were studied by the method of fluorescence resonance energy transfer with highly selective fluorescent probes. In contrast to 15-min coronary artery occlusion, 120-min ischemia was accompanied by irreversible structural and conformational changes in the small domain of erythrocyte actin. Posttranslational changes during myocardial ischemia concerned the N- and C-terminal regions of actin and went beyond the allowed conformational fluctuations in the actin molecule without breaking the energy barrier. Our results suggest that under conditions of ischemia, actin of the myocardium and erythrocyte cytoskeleton loses its ability to acquire conformation required for force generation by cardiomyocyte myofibrils and maintenance of elasticity and integrity of the erythrocyte membrane.

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Submolecular mechanisms underlying in vitro and in vivo effect of cardiac glycosides on contractile activity of myocardial myofibrils during heart failure

2006

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The development of severe heart failure associated with toxicoallergic myocarditis is accompanied by profound structural and conformational changes in the outer domain of actin (major protein in a thin filament of cardiomyocyte sarcomere). These changes were revealed in subdomains 1 (Cys374 and Cys10) and 2 (Lys61 and Tyr69). Structural and conformational changes in the monomer and protomer of the actin thread during heart failure were energetically forbidden. Variations in the distance between amino acid residues exceeded 0.26 nm. They were partly or completely reversible in vivo under the influence of cardiotropic drug refracterin with high antihypoxic activity, as well as in vitro after treatment with digitalis preparations optimizing the concentration of ATP.

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Cited by 6 publications

References 2 publications

Effect of NAD on recovery of adenine nucleotide pool, phosphorylation potential, and stimulation of apoptosis during late period of reperfusion damage to myocardium

Effect of NAD on recovery of adenine nucleotide pool, phosphorylation potential, and stimulation of apoptosis during late period of reperfusion damage to myocardium

Structural and Conformational Changes in Myocardial and Erythrocyte Actin during Cardiac Ischemia

Submolecular mechanisms underlying in vitro and in vivo effect of cardiac glycosides on contractile activity of myocardial myofibrils during heart failure

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