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J Moravec

Publications and source records attributed to J Moravec.

At least 55 records · Page 3Linked to original sources
PubMed1975

Dependence of myocardial redox systems on the concentration of exogenous substrate.

Isolated rat hearts were perfused according to Langendorff at a range of perfusion pressures and the variations of intracellular oxygenation were studied under these conditions by optical methods. The oxygen consumption was directly related to left ventricular performance in all cases examined, the relationship being independent of both the substrate used (glucose, beta-OH-butyrate) and its concentration (2.5, 5.0, 10.0 mM). The changes in the respiratory rate were accompanied by modifications of the redox state of mitochondrial enzyme systems (reduced nicotinamide adenine dinucleotide (NADH), cytochromes) in presence of low concentration (2.5 mM) of substrate. At higher substrate concentrations (5.0, 10.0 mM), however, no change in the redox state of cytochromes and only inconsistent fluctuations of that of NADH were observed. These results suggest that the generally accepted relationship between the rate of electron transport and the degree of reduction of respiratory coenzymes exists only under special conditions (low substrate concentration). Other factors, such as the size of the pool of hydrogen available, should be considered. Furthermore, this work specifies the optimal experimental conditions for the study of mitochondrial respiratory transitions (low substrate) in the intact myocardium by means of direct optical techniques.

Acetoacetates↗
PubMed1975

[The rat ventricular myocardium in chronic hypercapnia. Electron microscopic study].

An electron microscope study of the left ventricular myocardium from rat acclimatized to chronic hypercapnia was done in order to complete the preceding work concerning general effects of respiratory acidosis. After 15 and 30 days of the acclimatation to 8% CO2 no lesions of the myocardium could be found. The results of the morphometric analysis indicated, however, discrete modifications of heart ultrastructure similar to those found before in hypoxic and failing hearts: namely a decrease of mitochondrial mean diameter and a non significant decrease of mitochondrial fractional volume. The latter was accompanied by a significant decrease of myofibrillar mass. The presence of cellular oedema seems to be suggested by an increase of fractional volume of the cytosol. The mechanism of these changes is not easy to explain. Further work will be necessary to make a choice between two possibilities: (1) depressed contractility related to some direct effect of high pCO2 and (2) tissue hypoxia secondary to local effects of the former.

Animals↗