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Biomedical subjects

V G Tsyplenkova

Publications and source records attributed to V G Tsyplenkova.

At least 19 recordsLinked to original sources
PubMed2006

[Effect of ubiquinone on contractile function and antioxidant status of the myocardium in spontaneously hypertensive rats].

During the period of aging of spontaneously hypertensive rats (SHR) between 6 and 13 weeks the systolic arterial pressure increased from 131+/-2 up to 176+/-3 mm Hg while in the control group of WKY rats it reached 122+/-2 mmHg. The hypertension was combined with myocardial hypertrophy -- the relative weight of SHR heart was 24% higher. The contractile myocardial function of the isolated isovolumic heart of SHR group did not differ from WKY group in a wide range of coronary perfusion rates. During oxidative stress induced by 40-min intracoronary introduction of H(2)O(2) function of hypertrophied SHR hearts fell significantly deeper. This coincided with decreased myocardial activity of superoxide dismutase and glutathione peroxidase by 29-30%, and increased catalase activity by 18%. The rate of generation of active forms of oxygen (hydroxyl radicals HO(.-)) in mitochondria from SHR hearts was higher as compared with WKY. Thus, the development of hypertension was combined with decreased antioxidant protection of the myocardium. The addition of ubiquinone to drinking water (approximately 10 mg/kg/day) for 6 weeks did not affect arterial pressure level, but was associated with two times lesser degree of myocardial hypertrophy. The hearts of SHR that received ubiquinone differed from those not treated with ubiquinone by increased maximal level of myocardial contractile function, and by improved myocardial relaxability and distensibility. After administration of H(2)O(2), myocardial function of SHR was kept on higher level. That was combined with less myocardial oedema, better preservation of antioxidant enzymes and reduced rate of succinate-dependent generation of superoxide radicals in mitochondria from hearts of ubiquinone treated SHR. The results have shown, that administration of ubiquinone to rats with hereditary hypertension reduces degree of myocardial hypertrophy, improves functional properties of the myocardium, promotes effective protection of antioxidant enzymes and increases the resistance of the cardiac muscle to oxidative stress.

Animals↗
PubMed2004

Protection of rat myocardium by coenzyme Q during oxidative stress induced by hydrogen peroxide.

Ubiquinone Q(10) (coenzyme Q) is an important component of the mitochondrial electron transport chain and an antioxidant. The purpose of this work was to find out whether an increase in the level of coenzyme Q in the heart changes its maximal working capacity and resistance to oxidative stress. Male Wistar rats were treated with coenzyme Q (10 mg/kg body weight per day) for six weeks, and this increased its content in the myocardium by 63%. The myocardial content of malonic dialdehyde and activities of key antioxidant enzymes were unchanged, except nearly 2.5-fold decrease in the activity of superoxide dismutase. The maximal working capacity of the isolated isovolumic heart did not change, but under conditions of oxidative stress induced by 45-min infusion of hydrogen peroxide (70 micro M) into coronary vessels the contractile function of these hearts decreased significantly more slowly. This was associated with less pronounced lesions in the ultrastructure of cardiomyocytes and lesser disorders in the oxidative metabolism of mitochondria that suggested increased antioxidant protection of the myocardium.

Animals↗
PubMed2004

[Protective effect of hydrophilic ubiquinone on cardiac muscle during oxidative stress].

AIM: To assess effects of long term administration of a natural antioxidant ubiquinone on isoproterenol induced myocardial injury. METHODS: Rats were given hydrophilic ubiquinone with water for 8 weeks. RESULTS: Long term use of ubiquinone did not affect myocardial ultrastructure and relative myocardial weight. The dose of isoproterenol used in this study exerted moderate damaging action evidenced by disappearance of glycogen from sarcoplasm, development of edema, and partial destruction of mitochondrial cristae. These effects were associated with lowering of maximal magnitude of contractile function of the isolated heart and augmentation of superoxide radicals release in perfusate. These changes (except disappearance of glycogen) were not present in hearts of ubiquinone fed rats. Compared with controls mitochondria isolated from hearts of ubiquinone fed rats had higher respiratory control and more than twice lower rate of superoxide generation. CONCLUSION: As damaging effects of isoproterenol are mediated by augmented generation of active forms of oxygen the results obtained allow to suggest that myocardium of ubiquinone fed animals is characterized by elevated power of the antioxidant system.

Animals↗
PubMed2004

[Apoptosis and hibernation of cardiomyocytes of periscar zone as factor of chronic cardiac aneurysm progression].

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. Extent of apoptosis was different in aneurysms on different stages of organization. Number of altered cardiomyocytes was the greatest in immature aneurysms. Basing on these findings apoptosis of hibernating cardiomyocytes was suggested to be one of factors of expansion of sclerotic zone and aneurysm formation.

Apoptosis↗
PubMed2002

[The protective action of ubiquinone at ischemia and reperfusion].

Effects of prolonged consumption of ubiquinone on myocardial injury caused by ischemia and reperfusion were studied in reperfused rat hearts. Wistar rats received lipophylic or hydrophilic forms of ubiquinone for 6-8 weeks with chow or water, respectively. Isolated isovolumic hearts with a constant volume latex balloon in the left ventricular cavity were subjected to total normothermic ischemia (25 min) and subsequent reperfusion (50 min). Time course of ischemic contracture and its level in both groups of ubiquinone treated animals were similar to those in controls. However recovery of left ventricular developed pressure after reperfusion was significantly better in both ubiquinone groups (54-/+9, 65-/+7, and 24-/+4 mm Hg in animals treated with lipophylic and hydrophylic ubiquinone and controls, respectively, p<0.01). As a result the developed pressure and heart rate product reflecting maximal aerobic capacity of the heart was also better restored. Both ubiquinone groups demonstrated absence of increased coronary tone that was characteristic for control animals. Mitochondria isolated from reperfused hearts of ubiquinone treated rats showed better preservation of structure and respiratory control. Rate of succinate-dependent generation of superoxide radicals determined with a spin trap TIRON in mitochondria from hearts of rats treated with hydrophylic ubiquinone (35-/+8 mmol O(2) /min/g) was approximately twice lower (p<0.05) than in control group (74-/+12 mmol O(2) /min/g) while the value in lipophylic ubiquinone group (48-/+9 mmol O(2) /min/g) did not differ significantly from the control. The results evidence that prolonged consumption of water-soluble ubiquinone increases resistance of rat myocardium to injuring action of reperfusion.

Animals↗
PubMed2002

[Isoproterenol induced changes of protein expression and myocardial ultrastructure].

AIM: To elucidate alterations in myocardial ultrastructure and protein expression caused by isoproterenol. METHODS: Biochemical, immunohistochemical and electron microscopic studies of rat myocardium were carried out 2 hours and 3 weeks after single injections of isoproterenol (50 and 10 mg/kg). Relative content of myospecific proteins (KRP - kinase-related protein, desmin), cytoskeletal proteins (tubulin, vinculin, and myosin light chain kinase - MLCK) and extracellular matrix protein, fibronectin, was determined by immunoblotting. RESULTS: In 2 hours after injection of 50 mg/kg of isoproterenol destruction of some cardiomyocytes, contracture of myofibrils, and mild edema of intercellular space occurred; the content of KRP decreased by l6%, and that of tubulin, vinculin and fibronectin - by 27-29%. Reduced level of these proteins and also of MLCK persisted until 3 weeks after injection and was associated with altered cardiomyocyte ultrastructure. Glycogen granules were sparse, mitochondria contained arrow-like inclusions characteristic for calcium overload, huge mitochondria connected by specialized intermitochondrial contacts were present. Enlarged intercellular space contained areas of fibrosis with increased amount of type I and II collagens and fibronectin. Lower dose of isoproterenol (10 mg/kg) did not cause noticeable damaging action in the acute period, but in 3 weeks thickening of extracellular matrix occurred accompanied by increases of KRP and tubulin contents (by 26-32% compared with control level). Similar rise in expression of these proteins, and also of MLCK was observed after addition of isoproterenol to culture of chicken cardiomyocytes. CONCLUSION: These results indicate that even single injection of isoproterenol causes long lasting structural alterations in cardiac muscle accompanied by increased expression of extracellular matrix proteins as well as sarcoplasmic proteins apparently involved in the hypertrophic response of the cardiomyocytes.

Adrenergic beta-Agonists↗
PubMed2002

[Effect of adriamycin on expression and content of myocardial structural and regulatory proteins].

The biochemical and morphological study of the cytoskeleton and extracellular matrix of rat heart was carried out after single injection of adriamycin (2.2 or 0.44 mg/kg). Hearts were taken for the study after 2 hours and 3 weeks after injection. The light and electronic microscopy, immunohistochemical determination of type I, III and IV collagens and fibronectin using specific antibodies were implied for morphological study; electrophoresis and immunoblotting were implied for the determination of the content of some proteins of cardiomyocytes (KRP or telokin, desmin, tubulin and vinculin), and extracellular matrix (fibronectin) and vascular smooth muscle cells (MLCK, myosin light chain kinase). Adriamycin injection in the dose 2.2 mg/kg which is close to therapeutic and known to alter intracellular membranes approximately in the half of cardiomyocytes, did not influence the relative volume and structure of collagen network but distinctly reduced the density of fibronectin-distribution. The content of tubulin, fibronectin, MLCK and KRP was significantly decreased by 18-24%, while contents of desmin and vinculin were changed insignificantly. After 3 weeks, an increased density and extension of collagen network indicating the development of diffuse fibrosis were observed. Contents of tubulin and KRP were increased above control level by 50 and 20%, respectively. Similar hyperrestitution of tubulin, fibronectin and KRP content by 15-25% was determined after smaller dose of adriamycin (0.44 mg/kg). Only content of MLCK out of proteins studied remained at lower level in both groups by 25-34%. Isolated chick embryo cardiomyocytes subjected to adriamycin responded by increased level of KRP expression by 20% in 4 days while the level of tubulin expression remained unchanged. Results showed that damage of cardiomyocytes and extracellular matrix after single injection of adriamycin in the dose close to therapeutic was followed by increased expression of some proteins of cytoskeleton and extracellular matrix. KRP seems to play active role in this reparative response while the steadily reduced level of MLCK expression may disturb the control of coronary vessels.

Animals↗
PubMed2001

Mitochondria enter the nucleus (one further problem in chronic alcoholism).

Electron microscopy of cardiomyocytes of patients with hypertrophic and alcoholic cardiomyopathies revealed the presence of nuclei with mitochondria accumulated in their core. This was associated with chromatin displacement towards the core of the nucleus. No large-scale intermixing of the nuclear content with the cytosol was found, although in some sections there were disruptions in the nuclear envelop continuity. The entrance of mitochondria into the nucleus was modeled in rats that were given ethanol and the catalase inhibitor aminotriazole for 12 weeks. It is suggested that the entrance of mitochondria into the nucleus promotes both the attack of mitochondria by nuclear proteins and the attack of nuclear DNA and proteins by proteins of the mitochondrial intermembrane space.

Amitrole↗
PubMed2000

Morphological patterns of death by myocytes in arrhythmogenic right ventricular dysplasia.

There are two forms of nuclear loss from eukaryotic cells: biochemical DNA degradation in apoptosis and nuclear extrusion from the cell body as seen in mammalian erythroblasts. In biopsies of right ventricular myocardium from 8 patients with arrhythmogenic right ventricular dysplasia (ARVD), we found not only a terminal deoxynucleotidyl transferase-mediated digoxigenin-deoxyuridine triphosphate nick-end labeling (TUNEL)-positive nucleus in mononuclear myocytes, but also 1 or 2 TUNEL-positive nuclei in multinuclear myocytes. With electron microscopy, we found a nuclear dislocation to the cell periphery, followed by its extrusion into the extracellular space. Both the migration and extrusion of the nuclei of myocytes resemble the morphogenesis of human erythroblasts. Nuclear extrusion from myocytes may be another form of programmed cell death. In support of this possibility, we also found evidence of cytoplasmic degradation in right ventricular myocytes from our ARVD cases, a process similar to one often seen in developmental programmed cell death and differing from typical nuclear apoptosis. In our ARVD cases, we thus found several different patterns of cell death, all associated with initial preservation of the plasmalemma and avoidance of local inflammation. All these features may be different responses to common signals for selective non-necrotic (apoptotic) death of right ventricular myocytes.

Adult↗
PubMed1991

[Morphological study of the myocardium of mice infected with Coxsackie B1 virus during the treatment with an immunomodulating drug T-activin].

The study was undertaken to examine myocardial morphological alterations in mice treated with T-activin in different periods of viral myocarditis. Two-month BALB/C mice of both sexes were used in the experiments, which were intraperitoneally given 0.2 ml Coxsackie B1 virus in a titer of 10(-3)-10(-7) D50 ml. The material was taken 3, 5, 7, 9, 15, and 30 days following infection. Intact mice and animals given culture fluid were applied as controls. T-activin was subcutaneously injected in a dose of 0.2 ml at the rate of 0.01 mg per kg body weight on day 5 after virus infection for 5 days. The predominance of an alterative component of inflammation (dystrophic, necrobiotic and necrotic changes) over proliferative processes was ascertained to be common to all periods of infection. T-activin administration attenuated myocardial damage.

Adjuvants, Immunologic↗
PubMed1991

[A morphological analysis of the specimens obtained during endomyocardial biopsies in patients with a clinical diagnosis of dilated cardiomyopathy].

The authors summarize experience gained with a study of biopsy specimens obtained on endomyocardial biopsies from 88 patients with a clinical diagnosis of dilated cardiomyopathy. The diagnostic value of the study was equal to 70%. Dilated cardiomyopathy largely masked myocarditis and alcoholic cardiomyopathy which were diagnosed morphologically in 30 and 13% of the patients, respectively. No morphological alterations which would allow one to change the clinical diagnosis of dilated cardiomyopathy were discovered in 26% of cases. It has been shown that endomyocardial biopsy is an important tool of diagnosis. In order to introduce it on a broader scale, it is necessary that quantitative uniform criteria for the diagnosis of endomyocardial diseases, primarily myocarditis, be elaborated.

Adolescent↗
PubMed1991

[Diagnostic value of the endomyocardial biopsy in the cardiologic therapeutic clinic].

Literature and authors' own data on the diagnostic value of endomyocardial biopsy in cases with clinical diagnosis of dilatation cardiomyopathy are analysed. It is shown that due to this biopsy the diagnosis of more than 20 heart diseases becomes possible. Myocarditis, the diagnosis of which is particularly difficult, is most frequently masked under dilatation cardiomyopathy. Ultrastructural studies are of great importance allowing to diagnose a number of heart diseases including alcoholic cardiomyopathy and viral myocardial lesions. The authors advocate wider use of endomyocardial biopsy which is sufficiently safe and informative.

Adult↗
PubMed1990

[Experimental data on relations of viral myocarditis and dilated cardiomyopathy].

The aim of the given study is to simulate viral myocarditis (VMC) experimentally and to reveal morphologic evidences of its transformations into the dilatation cardiomyopathy (DCMP). Syrian golden hamsters were infected with Coxsackie B2 virus. Optical and electron microscopic morphological changes of myocardium showed the possible transformation of VMC into DCMP.

Animals↗
PubMed1990

[Therapeutic effect of antioxidant dibunol in experimental alcoholic cardiomyopathy].

Ultrastructure and peroxide metabolism of rat myocardium were studied after alcohol administration and partial inhibition of catalase with amino-triazole. There were obtained morphological pattern of alcoholic cardiomyopathy and activation of lipid peroxidation in myocardium under these experimental conditions. Cardiomyocyte ultrastructure and level of lipid peroxidation were improved after treatment with antioxidant-dibunol in high doses (40 and 100 mg/kg). These data indicate the main role of lipid peroxidation in the pathogenesis of alcoholic cardiomyopathy and possibility of its therapy with antioxidants.

Animals↗
PubMed1988

[A critical analysis of experimental models of alcoholic cardiomyopathy].

Numerous experimental data on alcoholic cardiomyopathy were reviewed and classified basing on the mode of alcohol taking: 1) voluntary alcoholization; 2) semivoluntary alcoholization; 3) forced introduction of alcohol. The advantages and shortcomings of the methods in similating alcoholic cardiomyopathy were assessed. Efforts were made to identify the underlying pathogenetic factors of the disease. The most perfect simulation was achieved in liquid alcohol diet (semivoluntary model) combined with inhibition of the defence enzymes of the myocardium, for instance, inhibition of catalase activity. Alcoholic cardiomyopathy is shown to develop more rapidly in high doses of ethanol and long-lasting alcoholization.

Administration, Inhalation↗
PubMed1988

[Effect of chronic alcoholism on the state of the microcirculatory bed of the myocardium].

Ultrastructure of myocardial capillaries of rats was studied in cases of chronic alcohol intoxication, experimental alcoholic cardiomyopathy (ACM) and its correction with antioxidants (vitamin E, dibunol). Alterations in the microcirculatory bed were similar in all groups of animals irrespective of disturbances in cardiomyocytes. Cardiomyocyte ultrastructure was improved after treatment with antioxidants, but capillary bed was the same as in untreated animals. High dibunol doses caused the onset of perivascular sclerosis. Disturbances in the microcirculatory bed are, probably, the first step in the determination of ACM pathogenesis and therapy of ACM must be directed at the correction of both alterations of cardiomyocytes and capillary bed.

Animals↗