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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
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↗
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↗