Effect of Natural Cytokine Complex on Metabolism of Smooth Muscle Cells in Myocardial Arteries under Normal Conditions and during Hemodynamic Overload.

Histoenzymological methods were employed to examine the effects of systemically administered natural cytokine complex including IL-1, IL-2, IL-6, TNFα, MIF, and TGFβ on metabolism of smooth muscle cells in intramural myocardial arteries under physiological conditions and during acute hemodynamic overload of the heart. Natural cytokine complex markedly inhibited metabolism of vascular smooth muscle cells under control conditions and during acute experimental aortal stenosis. In vascular smooth muscle cells, deceleration of tricarboxylic acid cycle, redistribution of the fluxes in glycolytic cascade and its inhibition, down-regulation of oxidation of free fatty acids and their metabolites, and inhibition of the shuttle systems and biosynthetic processes were observed.

Effects of Natural Cytokine Complex on the Myocardial Blood Flow in Normal and under Conditions of Increased Hemodynamic Load.

The effects of a natural complex of cytokines IL-1, IL-2, IL-6, TNF, MIF, and GTFβ on myocardial blood flow were studied under control conditions and during acute experimental aortal stenosis. Systemic administration of the cytokine complex under control conditions led to moderate impairment of the blood flow in the myocardium associated with plethora and perivascular edema. The number of functioning vessels in the myocardium significantly increased under these conditions, which reflected enhancement of the coronary blood flow.

Effect of Natural Cytokine Complex on the Structure and Metabolism of the Cardiac Conduction System in the Myocardium under Normally and Increased Hemodynamic Load.

Effect of natural complex of cytokines with activity of IL-1, IL-2, IL-6, TNF, MIF, and GTFβ on the structure and metabolism of conduction cardiomyocytes was assessed in the control and under acute experimental aortic stenosis. After systemic administration of the cytokine complex in the control, structural abnormalities were revealed in a relatively low number of conduction cardiomyocytes; their relative number increased in the left ventricle and interventricular septum. When the complex was administered against the background of aortic stenosis, morphological changes in the conduction system were seen in a significant number of cells with their plasma imbibition, especially in the left ventricle and interventricular septum.

Effect of the Natural Cytokine Complex on the Structure and Metabolism of Contractile Myocardium Normally and under Increased Hemodynamic Load.

Effect of natural complex of cytokines with activity of IL-1, IL-2, IL-6, TNF, MIF, GTFβ on the structure and metabolism of contractile ventricular cardiomyocytes was assessed in the control and under conditions of acute experimental aortic stenosis. Systemic administration of the complex in the control had no significant effect on myocardial morphology with low number of damaged cardiomyocytes and low degree of structural damage. Administration of the cytokine complex against the background of aortic stenosis did not exert any additional alterative effect on cardiomyocytes, structural damage of contractual nature was moderate.

Histoenzymological Characteristics of Smooth Muscle Cells in Myocardial Vessels: A Comparative Study under Conditions of Increased Left or Right Ventricular Afterload.

Histoenzymological methods were used to study metabolism of smooth muscle cells of intramural myocardial arteries during experimental aortic or pulmonary artery stenosis. Aortic stenosis was accompanied by changes in smooth muscles of the left ventricle manifested by deceleration of tricarboxylic acid cycle, inhibition of oxidation of free fatty acids and their metabolites, flux redistribution in the glycolytic cascade, and inhibition of shuttle systems and biosynthetic processes. Similar metabolic alterations were observed in vessels of the ventricular septum, but they were not revealed in vessels of the right ventricle (except glycolysis stimulation).

Histoenzymological characteristics of the heart conduction system: comparative study with left or right ventricle afterload.

Histoenzymological changes, indicating inhibition of the main metabolic processes, were found in the conduction cardiomyocytes of the left ventricle and ventricular septum in experimental stenosis of the aorta. The histoenzymological changes in the conduction system of both ventricles and ventricular septum were similar in experimental stenosis of the pulmonary artery and indicated primarily activation of glycolysis. The histoenzymological profile of conduction cardiomyocytes differed little in cases when the increase of the pressure load was complicated or not complicated by the development of heart failure, particularly in pulmonary artery stenosis.

Histoenzymology of the contractile myocardium in experimental pulmonary stenosis.

Metabolism of contractile cardiomyocyte in experimental pulmonary stenosis complicated or not complicated by heart failure was studied by histochemical methods. In pulmonary stenosis not complicated by heart failure, intensification of glycolysis, more intense oxidation of free fatty acids and their metabolites, and acceleration of the citric acid cycle were found in the contractile cardiomyocytes. In pulmonary stenosis complicated by heart failure, glycogen content in the myocardium was sharply decreased.

Histoenzymological characteristics of the contractile myocardium in experimental stenosis of the aorta.

Contractile cardiomyocyte metabolism was studied by histochemical methods in experimental stenosis of the aorta complicated and not by heart failure. Acceleration of the citric acid cycle, more intense oxidation of free fatty acids and their metabolites, glycolysis intensification, and higher activity of shuttle mechanisms were found in the contractile cardiomyocytes in stenosis of the aorta not complicated by heart failure. The presence of these metabolic shifts in the myocardium of all studied compartments suggests their association with not only more intense heart work, but also with the effects of total systems neurohumoral factors.

Pathomorphology of the heart conduction system: comparative study during increase in left or right ventricular afterload.

Pathomorphology of the peripheral compartments of the heart conduction system under conditions of increased left or right ventricular afterload is characterized by interstitial edema, hemorrhages, and reversible and irreversible focal lesions. The percentage of damaged conduction cardiomyocytes increases in the wall of hemodynamically overloaded ventricle and in the ventricular septum. These changes are more pronounced in cases when the afterload increase is complicated by heart failure development.

Pathomorphology of myocardial circulation: comparative study in increased left or right ventricle afterload.

Comparative study of pathomorphology of myocardial circulation under conditions of increased afterload of the left or right ventricles showed similar changes. All compartments of the coronary bed were plethoric, capillary blood stasis and perivascular edema, more pronounced in arterial vessels, were detected in both cases. These changes equally involved both ventricles and the ventricular septum.

Comparative pathomorphological study of contractile myocardium under conditions of increased left and right ventricular afterload.

Structural changes in the myocardium under conditions of increased left and right ventricular afterload were studied using polarization microscopy and histological, histochemical, and stereological methods. Increased afterload not complicated by heart failure was characterized by low number of damaged cardiomyocytes (3.3-6.

Structural and metabolic changes in cardiac conducting system during massive pulmonary embolism.

We studied structural and metabolic changes in ventricular conducting cardiomyocytes during the acute phase of massive pulmonary embolism complicated or uncomplicated by cardiac insufficiency. During massive pulmonary embolism without cardiac insufficiency, glycolysis in conducting cardiomyocytes of both ventricles was activated, and its contribution to energy formation increased. Massive pulmonary embolism complicated by cardiac insufficiency was accompanied by inhibition of glycolytic enzymes and damages to conducting cardiomyocytes of the left and right ventricles.