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Biomedical subjects

V Bada

Publications and source records attributed to V Bada.

51 records · Page 3Linked to original sources
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↗
PubMedDate not supplied

[Secondary prevention in patients after a myocardial infarct].

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 radicals, 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 significant 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.)

Humans↗