The release of calcium from cardiac mitochondria: The importance of the calcium-protein ratio

Göring, G; Nayler, Winifred G.; Spieckermann, P. G.

doi:10.1007/bf01906303

Cited by 3 publications

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References 12 publications

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“…The mitochondrial pellet was characterized in terms ultrastructure, P/O ratio, oxygen uptake, RCI-value as well as the cytochrome oxidase and succinic dehydrogenase activity (see 1,14). The concentration of protein in the final suspension was estimated by the biuret method and standardized against a commercially available protein-standard (Boehringer Mannheim).…”

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Ca2+-uptake and-release phenomena from cardiac mitochondria under normal and ischemic conditions

Göring

Spieckermann

1978

Basic Res Cardiol

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Guinea-pig and dog heart mitochondria were isolated in a KEA-medium. Ca2+-transport across mitochondrial membranes was measured continuously with an Aminco Dual-Wavelength-Spectrophotometer and murexide as a Ca2+-sensitive indicator. Ischemia was produced by cardioplegia at 15 degrees C according to Bretschneider. Guinea-pig heart mitochondria as well as mitochondria from dog heart show a spontaneous Ca2+-release without nonphysiological influence. Addition of 3.5 M Na+ can induce a very quick release of Ca2+ taken up by heart mitochondria. This release is different from that occurring spontaneously. Progressive ischemia results in a marked depression of Ca2+-uptake and spontaneous Ca2+-release.

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confidence: 99%

Ca2+-uptake and-release phenomena from cardiac mitochondria under normal and ischemic conditions

Göring

Spieckermann

1978

Basic Res Cardiol

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Functional alterations of cardiac subcellular structures during energy deficiency in relation to the metabolic state of the heart muscle cell

Spieckermann

Gebhard

Göring

et al. 1980

Experimental Cardiac Hypertrophy and Heart Failure

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Functional alterations of cardiac subcellular structures during energy deficiency in relation to the metabolic state of the heart muscle cell

et al. 1980

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The functional behaviour of membrane systems of the cardiac cell during oxygen deficiency was analyzed and the alterations were related to the metabolic state of the tissue as an index of injury. 1. The retention function of the cell membrane for proteins. With increasing energy deficiency the cardiac sarcolemma loses its ability to retain macromolecules (myoglobin, enzymes) within the cell. Close correlations exist between protein release and oxygen supply as well as ATP content of the tissue. 2. Function of isolated mitochondria after ischemia. In parallel with a strong impairment of oxidative phosphorylation (decrease of QO2, RCI values, phosphorylation rates) the Ca++-transporting activity of mitochondria is continuously depressed with decreasing myocardial ATP. 3. Function of isolated sarcoplasmic reticulum after ischemia. With breakdown of high energy phosphates during ischemia rate and extent of Ca++ binding with decrease markedly.

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The release of calcium from cardiac mitochondria: The importance of the calcium-protein ratio

Cited by 3 publications

References 12 publications

Ca2+-uptake and-release phenomena from cardiac mitochondria under normal and ischemic conditions

Ca2+-uptake and-release phenomena from cardiac mitochondria under normal and ischemic conditions

Functional alterations of cardiac subcellular structures during energy deficiency in relation to the metabolic state of the heart muscle cell

Functional alterations of cardiac subcellular structures during energy deficiency in relation to the metabolic state of the heart muscle cell

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