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Biomedical subjects

V Bada

Publications and source records attributed to V Bada.

At least 37 records · Page 2Linked to original sources
PubMed1984

Smoke cardiomyopathy: disturbance of oxidative processes in myocardial mitochondria.

The effect of inhalation of cigarette smoke (passive smoking) on the oxidative and phosphorylating processes of rabbit myocardial mitochondria was studied in three experimental models after a single smoke lasting 30 min, after 2 weeks smoking twice daily and after 8 weeks smoking twice daily. A significant decrease in respiration as well as in the phosphorylation rate of mitochondria was found; whereas the respiratory control index and coefficient of oxidative phosphorylation did not change. Both factors of cigarette smoke (carbon monoxide and nicotine) participate in the metabolic injury of mitochondria. Long term cigarette smoking causes considerable metabolic and morphological alterations to the heart muscle which can be characterised as smoke cardiomyopathy.

Animals↗
PubMed1982

The effect of cyclophosphamide on the myocardial oxidase system of mitochondria.

The authors studied the effect of immunosuppressive doses of cyclophosphamide (5 mg/kg b. w.) on the activity of myocardial NADH, succinate and cytochrome oxidases in the mitochondria of rabbit myocardium on two experimental models: a) after a single dose of cyclophosphamide (acute model); b) after cyclophosphamide given daily for a period of 10 weeks (chronic model). A single dose of cyclophosphamide did not affect the myocardial oxidase systems of mitochondria, whereas its chronic administration significantly increased the succinate oxidase activity and decreased cytochrome oxidase activity. The drug did not interfere with NADH- oxidase activity. It is concluded that long-term administration of cytostatic and immunosuppressive doses of cyclophosphamide may result in severe myocardial lesions on subcellular level. This should be taken into account in clinical practice.

Animals↗
PubMed1979

The effect of propranolol on myocardial oxidative processes.

The effect of single i. v. dosis of propranolol, 1.5 mg/kg of body weight, on the oxidative processes in rabbit myocardium at the mitochondrial level was investigated. Analyses were carried out at minutes 0 and 15 after intravenous infusion of propranolol. Under the influence of propranolol the mitochondrial oxygen uptake was reduced. This finding reveals the metabolic background of the antianginal effect of propranolol. Simultaneously, however, the mitochondrial metabolic efficiency was negatively affected, as manifested by decreases in mitochondrial respiration control, oxidative phosphorylation, and phosphorylation rate. The described changes signalize a disturbance in myocardial energy production and represent a subcellular metabolic background of potential myocardial damage during administration of propranolol.

Animals↗
PubMed1977

The effects of ethanol on myocardial mitochondrial and sarcoplasmic ATPase in rats.

The effects of the ethanol on the activities of mitochondrial and sarcoplasmic Mg2+-Ca2+-activated ATPase in rat myocardium were studied on two experimental alcoholic models: a) in an acute model - after a single dose of ethanol, 250 mg/100g of body weight; b) in a chronic model - after daily administration of the same dose for 10 weeks. In the acute model the ATPase activities sank both in mitochondria and sarcoplasmic reticulum. In the chronic model an opposite tendency was observed: in both subcellular organelles the ATPase activities moderately rose. The findings are assessed from the aspect of the dynamics of myocardial metabolic changes in dependence on the duration of action of ethanol upon the myocardium. It is stressed that acute symptoms of the ethanol action on myocardial metabolic processes are no adequate basis for drawing conclusions about the mechanism of myocardial lesion and the development of ethanol-induced mycardiopathy in chronic alcoholics.

Adenosine Triphosphatases↗
PubMed1975

[Problems of myocardiopathies in the clinical and experimental cardiology].

The first part of the study deals with the early diagnosis of cardiomyopathies on the ground of physical examination of the patients and of his ECG and X-ray finding. It is stressed, that in the majority of cases already this set of examination can in the physicial of the first contact awake a suspicion of cardiomyopathy. Further precision of diagnosis demands examination in a cardiological center where the facilities for cardiac catheterization, angiography and coronarogrpahy are available. The second part of the study deals with the problem of mechanism of the early heart failure in caridomyopathies. Studying the structural, metabolic and functional changes of the heart muscle in the dietetic, catecholamine and alkoholic model of experimental cardiomyopathy, the authors came to the conclusion that the main factor in this pathological event is disturbance of the oxidative process and thus of the energy generation at the subcellular level in the heart muscle. This metabolic disturbance is progressively leading to morphological changes and to a weaking of the contractile power of the heart muscle.

Angiography↗
PubMed1975

Myocardial cell damage due to ethanol.

The effect of ethanol on the myocardial metabolism of experimental animals was studied in acute and in chronic models. Thirty minutes after intraperitoneal injection of ethanol in a dose of 250 mg/100 gm of body weight there was a significant increase of glycolysis and slight decrease of mitochondrial respiration as well as of respiratory control ratio. No changes were observed in the concentration of high energy phosphates in the heart muscle. The metabolic changes in these acute experiments were of a transitory character; they disappeared parallel with the decline of ethanol level in the blood and in the myocardium. The chronic alcoholic model was observed for 10 weeks. Ethanol (250 mg/100 gm) was injected daily. The analyses of the heart muscle were carried out 24 hr after the last injection of ethanol. In this model ethanol also provoked considerable disturbances of metabolic processes in the myocardium: decrease of glycolysis and of glycogen content, decrease of mitochondrial respiration as well as of respiratory control ratio of isolated mitochondria and decrease of adenosine triphosphate and creatine phosphate with simultaneous increase of inorganic phosphate in the myocardium.

Adenosine Triphosphate↗