Gvozdják J

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. In conclusion, prolonged smoking may provoke myocardial dysfunction and in this way may contribute to the development of heart failure in chronic smokers.

Chronic effect of ethanol on the metabolism of myocardium

Abstract Chronic administration of ethanol (2.5 μ/kg for 10 weeks) to rats caused growth retardation, decrease of myocardial glycogen, and a decrease of myocardial homogenate respiration and of glycolytic activity. Heart mitochondrial respiration was slightly lowered but respiratory control decreased significantly. Heart weight was unchanged, as was blood glucose. These results are discussed with respect to the possibility of chronic damage to the heart muscle.

Effect of Ethanol on the Metabolism of the Myocardium and its Relationship to Development of Alcoholic Myocardiopathy

The effect of ethanol on the metabolism of the heart muscle was studied in two series of experiments in the rat. In an acute model, a single injection of 250 mg ethanol/l00 g body weight was given int

The effect of glucagon on the heart muscle: Relation between metabolic processes and contractility

Abstract The effect of glucagon on the contractility of the heart muscle (heart rate, left ventricular pressure, dp dt max ) as well as on the oxidative processes of myocardial mitochondria [respiration, respiratory control index, oxidative phosphorylation] and energy stores in the heart muscle [adenosine-triphosphate, creatine-phosphate, glycogen] of rabbits were studied. Glucagon (in the doses of 0.07 mg/kg of body wt) was administered to animals for 15 min. the parameters of contractility (mainly dp dt max ) increased. However, this effect of glucagon only lasted 15–20 min. the respiration of mitochondria simultaneously increased. It provoked neither damage of the mitochondria nor a deleterious situation in the energy stores of the myocardium. On the basis of these results the following conclusions were drawn: (1) Glucagon has a positive inotropic effect of short duration on the heart muscle. (2) In a parallel manner, it enhances oxidative processes in the myocardium at mitochondrial level. (3) It does not provoke either metabolic disturbances of the mitochondria or a deleterious energy situation in the myocardium, and (4) Glucagon is a favourable cardiotonic drug in the therapy of acute but not of chronic heart failure.

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. We explain these alterations of heart muscle metabolism at the mitochondrial level as an adaptation to the mild hypoxic conditions.

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.