Ruthenium Red

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Andrew M Keller - One of the best experts on this subject based on the ideXlab platform.

  • postischaemic reperfusion injury in the isolated rat heart effect of Ruthenium Red
    Cardiovascular Research, 1991
    Co-Authors: Vincent M Figueredo, Karl P Dresdner, Arlene C Wolney, Andrew M Keller
    Abstract:

    Study objective – The aim was to investigate the effect of attenuating mitochondrial calcium uptake with Ruthenium Red on myocardial function and the resultant necrosis following prolonged ischaemia and reperfusion in isolated rat hearts. Mitochondrial dysfunction, secondary to increased calcium uptake, has been implicated as an important mediator of reperfusion injury in the heart. Design – To examine the role of mitochondrial calcium uptake in mediating ischaemic and reperfusion injury, isolated rat hearts were perfused with Ruthenium Red (n=6), a polysaccharide dye which inhibits calcium uptake by mitochondria, and were compaRed to control perfused hearts (n=7). After stabilisation, hearts were subjected to 60 min no flow ischaemia, immediately followed by 40 min reperfusion. Experimental material – Hearts were used from male Wistar rats weighing 300-350 g. Measurements and main results – Cardiac high energy phosphates (ATP, phosphocreatine, inorganic phosphate) and pH were continuously monitoRed during ischaemia and reperfusion using phosphorus magnetic resonance spectroscopy. Contractility (dP/dT), coronary flow, creatine kinase release, and the time to the onset of ischaemic contracture were also measuRed. No differences in metabolic abnormalities or time to peak contraction during ischaemia were found between groups, suggesting that Ruthenium Red does not alter the metabolic consequences of ischaemia. However, upon reperfusion, the following differences in the Ruthenium Red perfused hearts were observed when compaRed to control hearts (p<0.05): ATP and phosphocreatine recovery were more complete, myocardial contractility was greater, coronary flow was greater, and myocyte necrosis was attenuated. Conclusions – Combined with the known inhibitory effect of Ruthenium Red on mitochondrial calcium uptake, these data suggest that an important component of myocardial injury following ischaemia and reperfusion in the isolated rat heart is the result of mitochondrial calcium accumulation.

Vincent M Figueredo - One of the best experts on this subject based on the ideXlab platform.

  • postischaemic reperfusion injury in the isolated rat heart effect of Ruthenium Red
    Cardiovascular Research, 1991
    Co-Authors: Vincent M Figueredo, Karl P Dresdner, Arlene C Wolney, Andrew M Keller
    Abstract:

    Study objective – The aim was to investigate the effect of attenuating mitochondrial calcium uptake with Ruthenium Red on myocardial function and the resultant necrosis following prolonged ischaemia and reperfusion in isolated rat hearts. Mitochondrial dysfunction, secondary to increased calcium uptake, has been implicated as an important mediator of reperfusion injury in the heart. Design – To examine the role of mitochondrial calcium uptake in mediating ischaemic and reperfusion injury, isolated rat hearts were perfused with Ruthenium Red (n=6), a polysaccharide dye which inhibits calcium uptake by mitochondria, and were compaRed to control perfused hearts (n=7). After stabilisation, hearts were subjected to 60 min no flow ischaemia, immediately followed by 40 min reperfusion. Experimental material – Hearts were used from male Wistar rats weighing 300-350 g. Measurements and main results – Cardiac high energy phosphates (ATP, phosphocreatine, inorganic phosphate) and pH were continuously monitoRed during ischaemia and reperfusion using phosphorus magnetic resonance spectroscopy. Contractility (dP/dT), coronary flow, creatine kinase release, and the time to the onset of ischaemic contracture were also measuRed. No differences in metabolic abnormalities or time to peak contraction during ischaemia were found between groups, suggesting that Ruthenium Red does not alter the metabolic consequences of ischaemia. However, upon reperfusion, the following differences in the Ruthenium Red perfused hearts were observed when compaRed to control hearts (p<0.05): ATP and phosphocreatine recovery were more complete, myocardial contractility was greater, coronary flow was greater, and myocyte necrosis was attenuated. Conclusions – Combined with the known inhibitory effect of Ruthenium Red on mitochondrial calcium uptake, these data suggest that an important component of myocardial injury following ischaemia and reperfusion in the isolated rat heart is the result of mitochondrial calcium accumulation.

Juan C. Gómez-fernández - One of the best experts on this subject based on the ideXlab platform.

  • Characterization of Ruthenium Red-binding sites of the Ca(2+)-ATPase from sarcoplasmic reticulum and their interaction with Ca(2+)-binding sites.
    Biochemical Journal, 1992
    Co-Authors: Senena Corbalán-garcía, Joséa. Teruel, Juan C. Gómez-fernández
    Abstract:

    Sarcoplasmic reticulum Ca(2+)-ATPase has previously been shown to bind and dissociate two Ca2+ ions in a sequential mode. This behaviour is confirmed here by inducing sequential Ca2+ dissociation with Ruthenium Red. Ruthenium Red binds to sarcoplasmic reticulum vesicles (6 nmol/mg) with a Kd = 2 microM, producing biphasic kinetics of Ca2+ dissociation from the Ca(2+)-ATPase, decreasing the affinity for Ca2+ binding. Studies on the effect of Ca2+ on Ruthenium Red binding indicate that Ruthenium Red does not bind to the high-affinity Ca(2+)-binding sites, as suggested by the following observations: (i) micromolar concentrations of Ca2+ do not significantly alter Ruthenium Red binding to the sarcoplasmic reticulum; (ii) quenching of the fluorescence of fluorescein 5'-isothiocyanate (FITC) bound to Ca(2+)-ATPase by Ruthenium Red (resembling Ruthenium Red binding) is not prevented by micromolar concentrations of Ca2+; (iii) quenching of FITC fluorescence by Ca2+ binding to the high-affinity sites is achieved even though Ruthenium Red is bound to the Ca(2+)-ATPase; and (iv) micromolar Ca2+ concentrations prevent inhibition of the ATP-hydrolytic capability by dicyclohexylcarbodi-imide modification, but Ruthenium Red does not. However, micromolar concentrations of lanthanides (La3+ and Tb3+) and millimolar concentrations of bivalent cations (Ca2+ and Mg2+) inhibit Ruthenium Red binding as well as quenching of FITC-labelled Ca(2+)-ATPase fluorescence by Ruthenium Red. Studies of Ruthenium Red binding to tryptic fragments of Ca(2+)-ATPase, as demonstrated by ligand blotting, indicate that Ruthenium Red does not bind to the A1 subfragment. Our observations suggest that Ruthenium Red might bind to a cation-binding site in Ca(2+)-ATPase inducing fast release of the last bound Ca2+ by interactions between the sites.

Arlene C Wolney - One of the best experts on this subject based on the ideXlab platform.

  • postischaemic reperfusion injury in the isolated rat heart effect of Ruthenium Red
    Cardiovascular Research, 1991
    Co-Authors: Vincent M Figueredo, Karl P Dresdner, Arlene C Wolney, Andrew M Keller
    Abstract:

    Study objective – The aim was to investigate the effect of attenuating mitochondrial calcium uptake with Ruthenium Red on myocardial function and the resultant necrosis following prolonged ischaemia and reperfusion in isolated rat hearts. Mitochondrial dysfunction, secondary to increased calcium uptake, has been implicated as an important mediator of reperfusion injury in the heart. Design – To examine the role of mitochondrial calcium uptake in mediating ischaemic and reperfusion injury, isolated rat hearts were perfused with Ruthenium Red (n=6), a polysaccharide dye which inhibits calcium uptake by mitochondria, and were compaRed to control perfused hearts (n=7). After stabilisation, hearts were subjected to 60 min no flow ischaemia, immediately followed by 40 min reperfusion. Experimental material – Hearts were used from male Wistar rats weighing 300-350 g. Measurements and main results – Cardiac high energy phosphates (ATP, phosphocreatine, inorganic phosphate) and pH were continuously monitoRed during ischaemia and reperfusion using phosphorus magnetic resonance spectroscopy. Contractility (dP/dT), coronary flow, creatine kinase release, and the time to the onset of ischaemic contracture were also measuRed. No differences in metabolic abnormalities or time to peak contraction during ischaemia were found between groups, suggesting that Ruthenium Red does not alter the metabolic consequences of ischaemia. However, upon reperfusion, the following differences in the Ruthenium Red perfused hearts were observed when compaRed to control hearts (p<0.05): ATP and phosphocreatine recovery were more complete, myocardial contractility was greater, coronary flow was greater, and myocyte necrosis was attenuated. Conclusions – Combined with the known inhibitory effect of Ruthenium Red on mitochondrial calcium uptake, these data suggest that an important component of myocardial injury following ischaemia and reperfusion in the isolated rat heart is the result of mitochondrial calcium accumulation.

Karl P Dresdner - One of the best experts on this subject based on the ideXlab platform.

  • postischaemic reperfusion injury in the isolated rat heart effect of Ruthenium Red
    Cardiovascular Research, 1991
    Co-Authors: Vincent M Figueredo, Karl P Dresdner, Arlene C Wolney, Andrew M Keller
    Abstract:

    Study objective – The aim was to investigate the effect of attenuating mitochondrial calcium uptake with Ruthenium Red on myocardial function and the resultant necrosis following prolonged ischaemia and reperfusion in isolated rat hearts. Mitochondrial dysfunction, secondary to increased calcium uptake, has been implicated as an important mediator of reperfusion injury in the heart. Design – To examine the role of mitochondrial calcium uptake in mediating ischaemic and reperfusion injury, isolated rat hearts were perfused with Ruthenium Red (n=6), a polysaccharide dye which inhibits calcium uptake by mitochondria, and were compaRed to control perfused hearts (n=7). After stabilisation, hearts were subjected to 60 min no flow ischaemia, immediately followed by 40 min reperfusion. Experimental material – Hearts were used from male Wistar rats weighing 300-350 g. Measurements and main results – Cardiac high energy phosphates (ATP, phosphocreatine, inorganic phosphate) and pH were continuously monitoRed during ischaemia and reperfusion using phosphorus magnetic resonance spectroscopy. Contractility (dP/dT), coronary flow, creatine kinase release, and the time to the onset of ischaemic contracture were also measuRed. No differences in metabolic abnormalities or time to peak contraction during ischaemia were found between groups, suggesting that Ruthenium Red does not alter the metabolic consequences of ischaemia. However, upon reperfusion, the following differences in the Ruthenium Red perfused hearts were observed when compaRed to control hearts (p<0.05): ATP and phosphocreatine recovery were more complete, myocardial contractility was greater, coronary flow was greater, and myocyte necrosis was attenuated. Conclusions – Combined with the known inhibitory effect of Ruthenium Red on mitochondrial calcium uptake, these data suggest that an important component of myocardial injury following ischaemia and reperfusion in the isolated rat heart is the result of mitochondrial calcium accumulation.