Publications by authors named "Cherpachenko N"

Morphometrical research of the atherosclerosis plaques (AP) instability and responsible for decreasing of their stability structure has been carried out by estimation of the instability index (II). II is a ratio between sum of destabilizing (lipids and macrophages) and stabilizing (collagen fibers and smooth muscular cells) AP structures. Segments of the coronary arteries were received from 45-65 years old man after a coronary artery bypass grafting.

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Aim: To study some particularly inadequately studied mechanisms for the development of coronary artery calcification (CAC), which are unassociated with calcified atheromatous masses of atherosclerotic plaques.

Subjects And Methods: . Endarterectomized coronary artery (CA) segments obtained during aortocoronary bypass surgery were pathomorphologically studied in 150 patients aged 49-72 years with coronary heart disease (CHD).

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The morphological manifestations of the pleiotropic effect of statins on the human aortic intima in atherosclerosis were studied. The aortic fragments from males aged 45-65 years, obtained at aortocoronary bypass surgery, served as a material. The thickness of the aortic intima and its levels of macrophages, smooth muscle cells (SMC), collagen fibers, and glycosaminoglycans (GAG) were measured in patients treated and untreated with statins.

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We carried out pathomorphological study of fragments of the thoracic aorta obtained at aorto coronary bypass surgery in order to elucidate effect of statins on lipid component of vascular wall using the system of computer processing and image analysis. Treatment of patients with ischemic heart disease with statins leads to decrease of area of aortic intima occupied by lipids. Most significant lipid lowering action of statins has been noted at initial stage of atherosclerosis - in primary extracellular lipoidosis, less significant - in fatty streaks with intracellular lipids, and least significantly pronounced - in fatty streaks with secondary lipoidosis formed as a result of degradation of foam cells.

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Synthesis of prostaglandin-synthetase at the stage of development of lipid spots and plaques is increased and the degree of this depends on the cell response. Increase of PgS depends on the number of cells in the intima and adventicia. Pg synthesis in vessels is decreasing at the stage at the fibrous plaques formation.

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To test the reparative capacity of stromal cells in myocardial infarction, rats were injected with granulocyte-monocyte-colony stimulating factor (GM-CSF) (leukomax), a cytokine known by its ability to raise a level of stromal cells in the blood, during first three days after coronary artery ligation. Only 10 of 17 rats (59%) survived 4 weeks in this group compared with 16 of 24 (67%) among rats not treated with leukomax. Echocardiographic and electromanometric studies showed that in both groups ventricular (LV) dilatation which developed during first hours after surgery persisted throughout 6-8 weeks and was combined with decreased ejection fraction and elevated LV end diastolic pressure.

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Tissue specimen from chronic aneurysms and adjacent myocardium obtained at aneurysmectomy and coronary bypass surgery from 46 patients were subjected to morphological study. Immunohistochemical methods and electronic microscopy were applied for detection of apoptosis and hibernation of cardiomyocytes in 11 cases and histochemical determination of activity of energetic enzymes succinate and lactate dehydrogenase was used in 5 cases. Cardiomyocytes from peri and intra scar layers of myocardium were found to be in a state of hibernation while some of them were in a state of apoptosis.

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Aim: To study morphological and functional state of mast cells from intima of the aorta and pulmonary artery associated with acute cardiovascular failure due to myocardial infarction.

Material: Vessels of 44 men who died of acute myocardial infarction at the age of 42-73 years.

Methods: Intimal cellular elements were analyzed in membranous preparations of intima and transverse cross-sections of vessels.

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We studied transverse cross-sections (5 mm apart) of coronary arteries of 45 men and women who died of acute myocardial infarction at the age of 41-79 years. Both stable and unstable atherosclerotic plaques were found in all cases. Stable plaques consisted of solid fibrous tissue with small amount of lipids and cellular elements.

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Atherosclerosis was found in all ascending aorta biopsies of 125 patients aged 42 to 65 years who underwent aortocoronary bypass surgery. Lipid spots only were found in 91.2% of cases, in 11 patients (8.

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A series of hydroxynaphthazarins has been synthesized. Some of them were found in in vivo experiments to be protectors of myocardium under ischemia-reperfusion and to reduce the infarction zone by 50% without any adverse effect. All compounds exhibit a moderate or small toxicity and are active in low doses.

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Human aorta was studied at early stages of atherosclerosis: intimal edema, first signs of lipoidosis, lipid spots and lipid plaques. Adhesion of Mn/Mp and lymphocytes to the aortal intima directly correlated with lipid deposits in the vascular wall. The number of mononuclear cells in the intima increased in parallel to progression of lipidosis.

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Immunomorphological and histochemical studies were carried out on the aorta serial sections of 20-40-year-old males. The results demonstrate that monocytes appear in the aortal intima after fat deposition. Intensification of lipoidosis in the aorta promotes an increase in monocyte count in the intima.

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Myocardial biopsies from patients with dilated cardiomyopathy (DCMP) were studied histochemically. The patients were divided into the following groups: 1) idiopathic DCMP; 2) patients with postmyocarditis DCMP (an increase of lymphocytic-macrophagal elements in the myocardium); 3) secondary DCMP against alcoholic myocardial damage. Idiopathic and secondary DCMP are characterized by the following enzymatic changes: a decrease in the activity of the majority of oxidation-reduction mitochondrial enzymes, normal or increased activity of malate dehydrogenase, increased activity of lysosomal and microsomal enzymes.

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Endomyocardial biopsies from 20 patients with dilated cardiomyopathy (DCMP) were studied histochemically. The decrease of the mitochondrial enzyme activity and increase of the activity of lysosomal and hydrolytic enzymes were found. These alterations reflect degenerative processes in cardiomyocytes followed by activation of their degradation and utilization.

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The activity of human myocardial enzymes in sudden coronary death (SCD) was quantitatively histochemically examined. The activity of succinate dehydrogenase (SDH), lactate dehydrogenase (LDH), beta-oxybutyrate dehydrogenase (beta-OBDH), alpha-glycerolphosphate dehydrogenase (alpha-GPDH), NAD-diaphorase (NAD-ase), and glucose-6-phosphate dehydrogenase (G-6-PDH) was measured on prompt autopsies (up to 3 hours of death onset). beta-OBDH and LDH showed an increase in activity in the myocardium from the subjects who had suddenly died from coronary heart disease without evident changes in the heart.

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On the material of early autopsies of the above patients the activity of the following myocardial enzymes was undergone the quantitative histochemical study: succinate, lactate, (beta-oxybutyrate, d-glycerophosphate, glucose 6-phosphate and alcohol dehydrogenase, NAD-diaphorase, catalase, phosphorylase. The increase of the activity of practically all enzymes studied was observed in the myocardial areas with no circulation disturbances. This increase was due to the moderate myocardial hypertrophy.

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Enzymes in the human myocardium following sudden death were examined for activity in a quantitative histoenzymological study, these were NAD-dependent dehadrogenases of succinate (SDG), lactate (LDG), beta-hydroxybutyrate (beta-HOBDG), alpha-glycerophosphate (alpha-GPDG), alcohol (ADG), glucoso-6-phosphate (G-6-PDG), and NAD-diaphorase (NADse), and catalase. Autopsies were performed within 3 h after death. beta-HOBDG and LDG were found to show an increase in activity in the cardiomyocytes of sudden death subjects with coronary heart disease without apparent changes.

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Quantitative histochemical assays of several enzymes (succinic, lactic, beta-hydroxybutyrate, alpha-glycerophosphate, and glucose-6-phosphate dehydrogenases, NAD diaphorase, and phosphorylase) in the myocardium of persons who had died suddenly with postinfarctional cardiosclerosis have failed to reveal any changes specific for this patient group. Direct correlations were established between the enzyme activities assayed, on the one hand, and the extent of myocardial hypertrophy and the signs of chronic heart failure, on the other. The activities of beta-hydroxybutyrate dehydrogenase and glucose-6-phosphate dehydrogenase, which are involved in fatty acid utilization and in the pentose phosphate pathway, were elevated in cases of moderate hypertrophy, as were those of all redox enzymes in cases of strongly marked hypertrophy, although they were reduced in cases with signs of chronic cardiac failure despite the presence of considerable myocardial hypertrophy.

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The effect of an opioid hormone (Leu-enkephalin analog Tyr-Dala-Gly-Phe-Leu-Arg) on the healing of myocardial infarction caused by the ligation of the descending branch of the rabbit left coronary artery has been investigated. The peptide was injected intraperitoneally at a dose of 10 micrograms/kg daily. Using light and electron microscopy, the peptide has been shown to exert a pronounced stimulating effect on the healing of the necrotic zone on days 3 and 7 of the experiment.

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Seven hundred fifty-two cases of instantaneous sudden cardiac death were studied. Alcoholic cardiomyopathy was found in 127 cases (16.9%), predominantly in men under age 50 (73%).

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The morphologic features of alcoholic cardiomyopathy in human sudden death compared with those of experimental alcoholic cardiomyopathy (6 weeks of alcohol administration and simultaneous inhibition of catalase activity) proved to be nearly identical. Regular and similar alterations in alcoholic cardiomyopathy in both human victims of sudden death and experimental rats are described as a complex of alterations characteristic of alcoholic cardiomyopathy. This complex of changes was used as the basis for morphologic diagnosis of endomyocardial biopsy in two groups of patients: I) chronic alcoholics (second to third stages), and II) patients with clinically diagnosed congestive cardiomyopathy.

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The effect of exogenous phosphocreatine on ischemic myocardium was studied in experimental infarction in rabbits and in total ischemia of pig heart tissue (in vitro). It is shown that single dose administration of phosphocreatine is followed by its rapid clearance from blood plasma (with a half lifetime of 4-6 min), but constantly high plasma concentration of phosphocreatine can be maintained by its intravenous infusion. When administered by this method into rabbits during experimental myocardial infarction, phosphocreatine reduces by 40% the size of the necrotic zone.

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