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V Bada

Publications and source records attributed to V Bada.

At least 19 recordsLinked to original sources
PubMed1999

[The effect of streptozotocin-induced diabetes in the neonatal period on hepatic mitochondrial bioenergetics in adult rats].

BACKGROUND: Previous experimental studies focused on the liver mitochondrial bioenergetic changes in diabetes mellitus type I induced in adult animals. Information about the effects of persisting neonataly induced diabetes mellitus type I on the mitochondrial bioenergetics are missing. AIM: The aim of the study was to assess the degree of diabetes mellitus compensation and parameters of oxidative phosphorylation in rats aged 3 months with DM persisting from neonatal period. METHODS: DM was induced in male Wistar rats by repeated intraperitoneal administration of streptozotocine 45 mg/kg on 2nd and 9th day after birth. The concentrations of glucose, glycosylated haemoglobin, fructosamine were detected in the blood and the concentration of cholesterol and triacylglycerols in the blood and liver tissue, respectively. After mitochondria isolation from the liver we measured parameters of oxidative phosphorylation by polarography using Clark oxygen electrode. RESULTS: In the group of neonataly induced DM the concentration of glucose (23.10 +/- 1.55 vs 8.3 +/- 0.56 mmol/l), glycosylated haemoglobin (6.04 +/- 1.17 vs 3.99 +/- 0.44%) and blood cholesterol concentration (2.15 +/- 0.11 vs 1.83 +/- 0.09 mmol/l) increased significantly (p < 0.001 and p < 0.005 for cholesterol) comparing to a group of healthy rats. No statistically significant differences were found in the remaining parameters when comparing these two groups. The parameters of oxidative phosphorylation were significantly (p < 0.001) decreased in the group with DM comparing to control group of healthy animals--the index of respiratory control (4.87 +/- 0.25 vs 9.57 +/- 0.34), the rate of oxygen consumption in the stage 3 in ADP presence (88.61 +/- 4.62 vs 165.08 +/- 4.5 natO.mg/protein/min) and phosphorylation rate (203.54 +/- 7.26 vs 332.87 +/- 7.39 nmolATP.mg/protein/min) with NAD substrate glutamate. Similar trend was also seen with FAD substrate succinate. The index of oxidative phosphorylation ADP:0 was not changed in both groups. CONCLUSIONS: In 3 months old rats with neonataly induced DM the development of steatosis was not observed and uncoupling of oxidative processes from phosphorylation did not appear. Energy production was sufficient enough for normal functions of the liver and to ensure all needs of the organism. (Tab. 4, Ref. 51.)

Aging↗
PubMed1998

[In Process Citation]

The confirmation of ischaemic disease of the heart increases the probability of death due to cardiovascular causes to more than 80%. The overcoming of myocardial infarction increases, according to the past AHA data, the risk of the origin of a new coronary episode 5 or 7 fold. The necessity of decreasing this risk in the frame of secondary prevention is therefore very urgent. The first assumption of success in secondary prevention resides in optimal therapy in the acute phase of myocardial infarction. The thrombolytic therapy is accompanied by risks of re-perfusion lesion implying from the increased production of free oxygen radical, activation of leukocytes, intracellular calcium overload at a current deficit in potassium and magnesium, the defects of coronary microcirculation, increased sympathetic activities general disturbances of energetic reserves in myocardium. Very significantly is an early stratification of patients after MI to those indicated to intervention / in case that the mass of ischaemic myocardium exceeds 20%, or if EF is below 40%, and to patients who regarding the low risk are manageable by conservative procedure. Both groups profit from the modification of classical risk factors (hypertension, smoking, hypercholesterolaemia). The values of cholesterol measured within the acute phase of myocardial infarction are not indicative, very often they are low. Finally, also in the later period with so-called adequate values of the total cholesterol, the patient after overcoming IM is increasingly under threat. The aim of secondary prevention is to reduce the chief pathogen, namely LDL cholesterol below 2.6 mmol/l, the level of HDL cholesterol on the opposite should be above 1.0 mmol/l. It is necessary to re-emphasize that the bioactive capacity is borne but by the oxidated form of LDL. Oxidative stress has a direct negative effect on vascular endothelium, and haemocoagulation potential, it participates in the metabolic X syndrome (insulin resistance, hyperinsulinaemia, defects in glucose tolerance, hypertriglyceridaemia, hypertension). (Ref. 41.)

Journal Article↗
PubMed1997

[Trends in alcohol consumption in relation to liver diseases in Slovakia 1973-1994].

The World Health Organisation warns before the increase in alcohol consumption and the proportional increase in ethyltoxic diseases which have taken place in past decades. Slovakia is included into the countries with the highest consumption of alcohol in Europe. The authors present a retrospective analysis of alcohol consumption from 1973 to 1994 in Slovakia according to the kinds of alcohol beverages, in a selected district and according to profession and family status. The epidemiologic analysis of the situation of alcohol consumption that is currently present in Slovakia is based on the data from wholesale and retail sale in relation to the prevalence and the mortality due to hepatic cirrhosis. The presented data was investigated by the Slovak Statistical Institute and the Institute of Medical Statistics of the Slovak Republic. Mortality due to hepatic cirrhosis has increased during the past 40 years 10-fold in men, and 4-fold in women. A severely increasing trend in alcohol consumption which had taken place prior to 1990 was succeeded by an abrupt decrease in pure alcohol consumption after 1990 (as much as by 21.2%). This decrease corresponds with the proportional decrease in the prevalence of chronic hepatopathies (by 35%) and with the decrease in mortality due to hepatic cirrhosis (by 20%). This phenomenon may be explained by the proportional increase in prices of alcoholic beverages. According to average yearly consumption of pure alcohol (p.a.) per capita, the consumption of spirits dominates when compared with the consumption of beer and wine. It is desirable to continue in the begun decreasing trend in alcohol consumption which is crucial in the procurement of primary, secondary as well as of tertiary preventions on both individual and population levels. (Tab. 1, Fig. 6, Ref. 19.)

Alcohol Drinking↗
PubMed1997

Effect of captopril on the development of left ventricular hypertrophy in rabbits with aortic insufficiency.

We investigated the effect of captopril on the growth of the left ventricle in an experimental model of aortic insufficiency. Four groups of rabbits were studied 28 days after experimental intervention: 1. control, 2. control with captopril (10 mg/kg/day), 3. aortic insufficiency, 4. aortic insufficiency with captopril (10 mg/kg/day). Aortic insufficiency induced hypertrophic growth of the left ventricle demonstrated by increased weight and ribonucleic acid (RNA) concentration. Administration of captopril only slightly attenuated the weight increase of the left ventricle and the increase in concentration of left ventricular RNA. However, captopril reduced the concentration of left ventricular deoxyribonucleic acid (DNA) both in the control and even more in the group with aortic insufficiency. The chronic haemodynamic overload enhanced mitochondrial respiration in the left ventricle which was not influenced by captopril. We conclude that captopril in the dose 10 mg/kg/day did not prevent hypertrophy of the left ventricle but reduced left ventricular DNA concentration.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1996

[Cardiomyopathies from the aspect of clinical and experimental cardiology].

The study represents a summary of the latest experience, definitions, classification and diagnostics in cardiomyopathologic diseases. The main attention is drawn to the pathogenesis of cardiomyopathies, especially regarding the metabolic disturbances of the cardiac muscle on the mitochondrial level: the disturbances of oxidative and related energetic processes which the authors have registered in coincidence with the cardiomyopathological alcohol and smoking experimental model. The conclusion includes a notice about the prospective possibility for human cardiology to study these metabolic disturbances in endomyocardial biopsies in order to assess the diagnosis in early thus still reversible stages.

Cardiomyopathies↗
PubMed1996

[The effect of an alpha-tocopherol analog, MDL 73404, on myocardial bioenergetics].

The authors investigated the effect of the synthetic analogue of MDL 73,404 alpha-tocopherol on bioenergetic processes of the cardiac muscle in a control group of rats. After a 10-day application of the presented preparation they analyzed the following parameters of energetic metabolism: ATP, ADP, AMP and inorganic phosphorus. Beside these, the authors investigate the levels of main indicators of the purine metabolism (xanthine, hypoxanthine, inosine and uric acid) in the myocardium. Under the influence of the given analogue of alpha-tocopherol a significant increase in ATP, ADP and hypoxanthine took place in the myocardium. Also the total concentration of adenine nucleotide and relative ATP/ADP ratio increased in the cardiac muscle. On the basis of the gained results the authors came to a conclusion that the synthetic analogue of alpha-tocopherol MDL 73,404 has a favourable effect on the bioenergetic conditions in the myocardium. MDL 73,404 has a favourable cardioprotective effect on the cardiac muscle assumedly by means of stabilization of mitochondrial membranes on the myocardium with a subsequent impact on cellular ATP concentration.

Adenine Nucleotides↗
PubMed1996

[The cytoprotective effect of magnesium in global myocardial ischemia].

BACKGROUND: Administration of magnesium in the therapy of ischaemic heart diseases does not belong to the standard procedures. The results of clinical trials with application of this cation are mutually contradictive, mechanisms of its effect are not solved yet. Many physicians consider magnesium to represent a classical placebo, or an uncertain light sedative. MAIN PURPOSE AND OBJECTIVES: The study is aimed at proving the direct effect of magnesium on the heart muscle under ischaemic conditions which exclude the placebo effects. These conditions are mostly fulfilled by the model of isolated heart. MATERIAL AND METHODS: The authors used isolated rabbit hearts according to Langedorff with Krebs-Henseleit (KH) perfusion solution, the only variable of which is represented by concentration of magnesium. The following groups of patients were formed: 1. Control group-30-minute perfusion with normal Mg concentration (0.5 mmol/l) in KH solution. 2. Hypomagnesemia-30-minute perfusion with KH solution Mg-free. 3. Normomagnesemia+ischaemia-30-minute perfusion with normal concentration succeeded by a 60-minute global ischaemia. 4. Hypomagnesiaemia+ischaemia-30-minute perfusion with KH solution magnesium-free succeeded by a 60-minute global ischaemia. 5. Hypermagnesiemia +ischaemia-30-minute perfusion with increased Mg concentration in KH solution to 2.0 mmol/l succeeded by a 60-minute global ischaemia. The investigated parameters: after completion of perfusion the authors isolated mitochondria and evaluated individual parameters of oxidative phosphorylation by means of oxygraph/Gilson/with Clark's oxygen electrode. The calcium uptake by mitochondria was observed by means of calcium-sensitive electrode Orion (oxygraph Gilson). The formation of free oxygen radicals was observed indirectly by spectrophotometric assessment of malondialdehyde production. Concentration of mitochondrial nucleotides (AMP, ADP, ATP) was assessed by using HPLC. RESULTS: Hypomagnesemia lasting 30 minutes had a negative effect on the index of oxidative phosphorylation (ADP:O p < 0.005) the uptake of calcium (p < 0.002), ATP concentration in mitochondrial ATP (p < 0.05) and the production of free radicals significantly increased (p < 0.001). Normomagnesemia indicated practically no cytoprotective effect before global ischaemia of myocardium lasting for 60 minutes. Hypermagnesemia indicated a direct cytoprotective effect before global ischaemia affecting respiration of isolated heart mitochondria in state of S3 (p < 0.001), respiration control index RCI (p < 0.001), the rate of oxidative phosphorylation OPR (p < 0.001) and on the index of oxidative phosphorylation ADP:O (p < 0.05) on the uptake of calcium by mitochondria (p < 0.002) and on concentration of mitochondrial nucleotides ATP (p < 0.002). It was remarkable that also under conditions of moderate hypomagnesemia the production of malondialdehyde increased. CONCLUSIONS: Under our experimental conditions it was confirmed that magnesium yields direct cytoprotective effect on the subcellular level of the myocardium prior to global ischaemia, providing the process takes place under the condition of hypermagnesemia. (Tab. 1, Fig. 12, Ref. 45.) Key words: hypomagnesemia, normomagnesemia, hypermagnesemia, Langendorff's global ischaemia, mitochondrial metabolism, cytoprotective effect.

Adenosine Triphosphate↗
PubMed1995

[Cardiomyopathies and myocarditis].

The authors discuss recent findings regarding cardiomyopathies, assembled recently due to the association of clinical and experimental cardiology. The main attention is paid to the pathogenesis of cardiomyopathies from the aspect of metabolic disorders of the heart muscle at the cellular and subcellular level. The differential diagnosis in relation to myocarditis is still a serious problem in cardiology: acute myocarditis is not a myocardiopathy, there exists, however, a close relationship between viral myocarditis and the development of dilatation cardiomyopathies. Echocardiography is one of the most important diagnostic examinations.

Animals↗
PubMed1994

[New findings on cardiomyopathies].

In this review the authors summarize the newest knowledge on cardiomyopathies, which was obtained during the last ten years due to joint experimental and clinical in this field. It concerns the pathogenesis of cardiomyopathies from the point of view of metabolic damage of the heart on the cellular and subcellular level, the diagnosis--mainly by means of echocardiographic investigation, as well as the therapy of cardiomyopathies--medicamental and surgical (transplantation of the heart). (Ref. 6.)

Cardiomyopathies↗
PubMed1989

[Smokers' mitochondrial cardiomyopathy].

The authors analyze the metabolic background of mitochondrial myopathies of the skeletal musculature in humans. They summarize their results assembled over years pertaining to functional disorders of mitochondria of the heart muscle in experimental models of passive smoking in rabbits. Based on comparison of these disorders with disorders in mitochondrial myopathies they reach the conclusion that the concept of smokers' mitochondrial myopathy is justified.

Animals↗
PubMed1989

Cardioprotective effect of metipranolol on ischemic heart muscle.

The effect of the beta-adrenoceptor antagonist metipranolol given twice daily in a dose of 0.5 mg/kg body weight for 3 days on respiration, respiratory control index of mitochondria and oxidative phosphorylation was measured in the heart muscle of anesthetized dogs after 60 min of induced ischemia. In control animals pretreated with saline, all measured variables with the exception of the coefficient of oxidative phosphorylation were significantly decreased. In contrast, pretreatment with metipranolol significantly improved all measured myocardial metabolic variables. The effect of metipranolol on the oxidative phosphorylating processes was more pronounced when the metabolic substrate was glutamate than when it was pyruvate.

Animals↗
PubMed1989

Metabolic disorders of cardiac muscle in alcoholic and smoke cardiomyopathy.

The acute and prolonged effects of alcohol and smoking on the oxidative and energy processes of cardiac muscle in experimental animals were studied at the subcellular level. The acute effect of alcohol manifested itself by decreasing mitochondrial respiration, compensated by increased glycolytic activity of the myocardium so that myocardial energy phosphate concentration remained unchanged. The prolonged effect of alcohol (for a period of 14 days) resulted in a decrease in oxidative processes as well as in glycolytic activity with a subsequent decline in myocardial ATP and CP levels. Smoking led to a significant decrease in oxidative and total bioenergetic processes of cardiac muscle mitochondria both after acute and prolonged smoking. This metabolic disorder is localized in the terminal segment of the respiratory chain of the mitochondria at the level of cytochrome oxidase. The authors conclude that the above-mentioned disorders may play a role in the development of heart failure on the basis of alcoholic or smoke cardiomyopathy.

Animals↗
PubMed1987

The effect of smoking on myocardial metabolism.

The effect of passive smoking by the rabbits on the metabolism of myocardium was studied in three experimental models: following a single instance of smoking (for a period of thirty minutes); following a two-week smoking (twice a day for thirty minutes each); following an eight-week smoking (twice a day for thirty minutes each, i. e. for a period of 56 days. In isolated mitochondria of myocardium a decreased respiration, oxidative phosphorylation rates and cytochromoxidase activity were observed both after a single-instance smoking and prolonged smoking. The above disorders are closely related to the energy production in myocardium. Based on comparison of the above metabolic disorders with the changes in ultrastructure and myocardial function (described in the literature) the authors have come to the conclusion that the term "smoker's cardiomyopathy" which may develop in habitual smokers is well justified. This kind of cardiomyopathy may participate in the development of cardiac insufficiency even in the absence of atherosclerotic changes in the coronary arteries.

Animals↗