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P Mathes

Publications and source records attributed to P Mathes.

84 records · Page 5Linked to original sources
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[The calcium metabolism of myocardial mitochondria and sarcoplasmic reticulum in experimental potassium deficiency (author's transl)].

Mechanical Parameters of the whole, Langendorff-perfused cat heart and of isolated right ventricular papillary muscles are depressed in chronic potassium deficiency. 45Ca binding of sarcoplasmic reticulum (SR) was found to be diminished and correlated with a reduced contractility of the perfused hearts. 45Ca uptake of sarcoplasmic reticulum isolated from potassium deficient hearts was also reduced. The mitrochondrial 45Ca binding and endogenous Ca concentration were increased and there was a positive correlation between these two parameters. The data suggest that a reduced SR Ca binding plays a role in the depression of myocardial contractility in chronic potassium deficiency. Increased mitochondrial 45Ca binding in the presence of reduced 45Ca binding and uptake of sarcoplasmic reticulum suggests the possibility that mitochondria are an additional myocardial calcium pool in chronic potassium deficiency.

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Morphology and mitochondrial function of the surviving myocardium following myocardial infarction in the cat.

The surviving myocardium of the cat was studied 7 days and 6 weeks following experimental infarction. Seven days after infarction, ultrastructural alterations of the mitochondria indicative of slight hypoxic injury--clearing of the matrix and loss of dense matrix granules--were found. Together with intracellular edema and glycogen depletion this result was considered as a sign of relative hypoxia in the surviving myocardium 7 days after infarction. At the same time beta-glucuronidase activity of tissue homogenates was found to be elevated. Focal ischemic lesions in remote myocardium which have been described by other authors (5, 6, 23) were not detected in our experiments. Six weeks after infarction, the fractional volume occupied by myofibrils had increased whereas the fractional volume of mitochondria had remained unchanged (left ventricle) resp. had decreased (right ventricle). There were no qualitative changes detectable at the ultrastructural level. Based on the morphometric investigation of Anversa (1, 2), our results were regarded indicative of mild compensatory hypertrophy of the surviving myocardium. Glutamate dehydrogenase activity of tissue homogenates was shown to be increased when compared to control values. Furthermore our morphometric results showed that the unit mass of mitochondria has to render an enhanced amount of energy six weeks after infarction which might leave the surviving myocardium with a higher susceptibility to future hypoxic injury.

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