Passive smoking impairs endothelium-dependent relaxation of isolated rabbit arteries.

The aim of the present study was to examine the effect of prolonged passive smoking (lasting 3 weeks) on plasma catecholamine levels and reactivity of isolated rabbit arteries. Plasma noradrenaline, adrenaline and dopamine levels were determined radioenzymatically. Isolated rings of the thoracic aorta and carotid artery were suspended in organ chambers and connected to a force transducer for the recording of isometric tension.

[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.

[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 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.

[Redox therapy in mitochondrial diseases using coenzyme Q10].

Background: The biochemical and genetic analysis served as the basis for the definition of the following mitochondrial diseases (mt diseases) and the diseases of the mitochondrial deoxyribonucleic acid (mtDNA diseases): mitochondrial myopathy, encephalomyopathy, and cardiomyopathy. The therapy of mitochondrial diseases (in both practice and experiment) belongs to the current trends of research.

Aim: The study does not present any new experimental results but in their literary review the authors indicate: a) new trend in biochemical studies of mitochondrial diseases, b) some current knowledge on mtDNA diseases, c) the current trend of mitochondrial disease "redox therapy" by CoQ10, d) significance of the therapeutic task of CoQ10 in four experimental models of the myocardial mitochondria impairment (by ageing, smoking, alcohol, ischemia).

[Significance of mitochondrial Ca2+ transport in ischemic injury and myocardial protection].

The role of calcium regarding the origin of irreversible impairment of the myocardial tissue is being intensively studied. An important role in this process is played by mitochondria which by means of the active Ca2+ uptake stimulate its oxidative metabolism and intervene into the Ca2+ homeostasis in mitochondrial cells. The study investigates the influence of cardioprotective substances with distinct mechanisms of the mitochondrial Ca2+ uptake effect.

[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.

[Alcoholic mitochondrial cardiomyopathy].

The effect of alcohol on oxidative phosphorylation, activity of cytochrome oxidase and the content of cytochromes in mitochondria of the heart muscle was studied in rabbits after 14- and 21-day subcutaneous administration of 20% alcohol solution. Alcohol was found to exert an inhibitory effect on oxygen consumption and on the rate of energy production in mitochondria of the heart muscle, to decrease the specific activity of cytochrome oxidase and to increase the cytochrome content in the mitochondria. The authors classify these metabolic derangements under the concept of alcoholic mitochondrial cardiomyopathy and discuss broader aspects of mitochondrial diseases in medicine.

Metabolic adaptation of myocardial mitochondria to mild altitude hypoxia.

We studied the metabolic parameters of myocardial mitochondria (respiration, respiratory control index, oxidative phosphorylation rapidity and coefficient of oxidative phosphorylation) in two groups of rats: one living at an altitude of 140 m above sea level (control group) and the other living from birth at an altitude of 1350 m above sea level for 2 and 4 months (experimental group). Compared with the control rats, the experimental rats during 2 and 4 months of mild altitude acclimatization increased their basal and stimulated respiration, as well as the rapidity of energy production by myocardial mitochondria. The coefficient of oxidative phosphorylation under mild altitude hypoxia decreased but the respiratory control index did not change.

[The role of mitochondrial energy metabolism and oxygen free radicals in the pathogenesis of experimental autoimmune myocarditis].

In a model of autoimmune myocarditis in guinea piga, the authors studied energy producing processes in mitochondria and the role of oxygen free radical generation in tissue injury. A significant decrease in the capacity of oxidative phosphorylation was detected in parameters QO2 (S3) on the basis of glutamate + malate (p < 0.005) and pyruvate (p < 0.

[A model of autoimmune myocarditis in guinea pigs].

A model of autoimmune myocarditis was developed in guinea pigs. The disease was induced by repeated subcutaneous administration of heterologous myocardial tissue and adjuvants. After immunization all experimental animals developed myocarditis, mostly of diffuse but also of focal character of the inflammatory process.

Effect of smoking on the oxidative processes of cardiomyocytes.

The effect of prolonged (14 days) passive smoking on the respiration of isolated cardiomyocytes in rabbits using various substrates (pyruvate, glutamate, succinate) was studied. The endogenous respiration of cardiomyocytes was not affected whereas stimulated respiration as well as the ratio of stimulated to endogenous respiration significantly decreased. These results complement previous studies in which the effect of smoking on the metabolic processes of heart muscle mitochondria was measured.

[The effect of alcohol on the mitochondrial respiratory chain in the cardiac muscle].

The authors investigated the action of prolonged 2- and 3-week action of ethanol on the main parameters of oxidative processes and on the cytochrome content of mitochondria in the heart muscle in 3-month-old rats. They found a statistically significant reduction of the oxidative phosphorylation coefficient, the rate of energy formation and a transient increase of the cytochrome oxidase activity in mitochondria. Under these experimental conditions an increase of cytochromes (cyt aa3, b, c, c1, bc1, c + c1) in mitochondria of the heart muscle occurred.

The functional state of the creatine kinase system of myocardial mitochondria in alcoholic cardiomyopathy.

The authors studied the chronic effect of ethanol on the functional state of creatine kinase system in myocardial mitochondria of adult rats. Mitochondrial functions were determined in skinned fibres prepared according to Veksler without mitochondria isolation. Compared with control values, ethanol was found to decrease statistically significantly the velocity of creatine-stimulated mitochondrial respiration (Vcr) and that of maximum ADP-induced stimulation of mitochondrial respiration (Vmax).

Use of myocardial skinned fibres for the study of mitochondrial oxidative phosphorylation during ischaemia.

The authors studied mitochondrial oxidative phosphorylation in the skinned myocardial fibres of the rat and the rabbit during ischaemia. Saponin action on tissue was used to remove the sarcolemma while leaving the interior of intracellular structures intact. Mitochondrial oxidative phosphorylation was measured by polarography using Clark's oxygen electrode in the presence of NAD- and FAD-substrates.

[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.

[Left ventricular function in patients with recent onset of type I diabetes mellitus].

Left ventricular heart function was investigated by means of two dimensional (2D) echocardiography and pulsed Doppler (PD) echocardiography in 17 young consecutive patients aged 17-38 years (mean 26.6 y.) with type I diabetes mellitus of short duration (mean 5.

[Use of 35-lead mapping of the precordium in the evaluation of left ventricular function in patients after myocardial infarct].

The aim of the investigation was to assess the ejection fraction and regional wall dyssynergy from 35-lead precordial or trunk back ECG taken from 18 consecutive patients after anterior and/or posterior myocardial infarction two months after the acute episode. The percentages of Q waves (% Q) and scores of Q and/or QS waves obtained from 35-lead ECG were compared with the ejection fraction and regional wall dyssynergy recorded by 2D echocardiography. A very good correlation (r = 0.

[The effect of passive smoking and alcohol on cardiomyocytes in rabbits].

The authors investigated the action of two weeks' simultaneous action of passive smoking (breathing the smoke of three cigarettes for 30 minutes twice a day) and alcohol (5 ml 20% ethanol per 1 kg body weight s.c. twice a day) on the vitality of isolated myocytes of the rabbit heart muscle.

[The relation of myocarditis to the development of cardiomyopathy].

Dilated cardiomyopathy is a degenerative disease of the myocardium of unknown etiology. Evidence was provided in experiments on mice that it may develop as a late consequence of viral myocarditis. In experiments on mice it was also found that the damaging factor in the pathogenesis of myocarditis may be a reaction of the immune system rather than an infective agent.

[The effect of smoking and alcohol on oxidative phosphorylation in mitochondria in the myocardium].

The simultaneous effect of passive smoking and alcohol on oxidative phosphorylation was studied in rabbits after 14 day exposure. The results were compared with those obtained in previous studies on the isolated noxious effect of smoking or alcohol. The authors conclude that under the given experimental conditions the combined effect of ethanol and smoking doses not affect oxidative phosphorylation of mitochondria: energy production and respiration of mitochondria were preserved.

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.