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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1 Pt 2
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pubmed:dateCreated |
1998-2-23
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pubmed:abstractText |
Pyruvate has been shown to be a metabolic inotrope in the myocardium. In millimolar concentrations, it has been shown to increase both myocardial phosphorylation potential and the cytosolic [NAD+]-to-[NADH] ratio. To determine if changes in these parameters can alter intracellular Ca2+ concentration ([Ca2+]i) and hence contractile function, Ca2+ transients and cell shortening (CS) were measured in isolated rat ventricular myocytes superfused with a physiological N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid buffer (11 mmol/l glucose) with and without additional pyruvate, L-lactate, acetate, or isoproterenol. The addition of 5 mmol/l pyruvate resulted in a 33% increase in CS and a 39% increase in systolic [Ca2+]i. These pyruvate effects were 70% of those observed with 100 nmol/l isoproterenol. The mitochondrial monocarboxylate transport inhibitor alpha-cyano-4-hydroxycinnamate (250 mumol/l) strongly inhibited pyruvate inotropy, suggesting a substantial obligatory coupling between pyruvate inotropism and its oxidation by the mitochondria. A possible role of the cytosolic [NAD+]-to-[NADH] ratio was assessed by comparing the effects of 20 mmol/l L-lactate to those of equimolar pyruvate. In contrast to 20 mmol/l pyruvate, excess L-lactate failed to appreciably increase CS or systolic [Ca2+]i. The findings imply that, at levels substantially above 5 mmol/l, a portion of pyruvate inotropism might be due to extreme cytosolic [NAD+]-to-[NADH] ratios. This study is the first evidence that augmented [Ca2+]i transients are most likely the mechanism of cardiac pyruvate inotropism.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/Lactic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/NAD,
http://linkedlifedata.com/resource/pubmed/chemical/NADP,
http://linkedlifedata.com/resource/pubmed/chemical/Pyruvic Acid
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0002-9513
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
274
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
H8-17
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:9458846-Animals,
pubmed-meshheading:9458846-Calcium,
pubmed-meshheading:9458846-Cells, Cultured,
pubmed-meshheading:9458846-Cytosol,
pubmed-meshheading:9458846-Glucose,
pubmed-meshheading:9458846-Heart,
pubmed-meshheading:9458846-Heart Ventricles,
pubmed-meshheading:9458846-Lactic Acid,
pubmed-meshheading:9458846-Male,
pubmed-meshheading:9458846-Mitochondria, Heart,
pubmed-meshheading:9458846-Models, Cardiovascular,
pubmed-meshheading:9458846-Myocardial Contraction,
pubmed-meshheading:9458846-Myocardium,
pubmed-meshheading:9458846-NAD,
pubmed-meshheading:9458846-NADP,
pubmed-meshheading:9458846-Phosphorylation,
pubmed-meshheading:9458846-Pyruvic Acid,
pubmed-meshheading:9458846-Rats,
pubmed-meshheading:9458846-Rats, Wistar
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pubmed:year |
1998
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pubmed:articleTitle |
Pyruvate augments calcium transients and cell shortening in rat ventricular myocytes.
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pubmed:affiliation |
Division of Cardiothoracic Surgery, University of Wisconsin School of Medicine, Madison 53792-0001, USA.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, U.S. Gov't, P.H.S.
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