Source:http://linkedlifedata.com/resource/pubmed/id/16540370
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
7
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pubmed:dateCreated |
2006-10-30
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pubmed:abstractText |
We investigated the hypothesis that increased intracellular [Na+]i in heart failure contributes to preservation of SR Ca2+ load which may become particularly evident at slow heart rates. [Na+]i in SBFI-loaded myocytes from rabbits with pacing-induced heart failure (PHF) was significantly higher at each frequency as compared to Sham-operated animals. Furthermore, PHF rabbits demonstrated reduced SR Ca2+-ATPase protein levels (-37%, p < 0.04) but unchanged Na+/Ca2+ exchanger protein levels. At 0.25 Hz, isometric force was similar in cardiac trabeculae from PHF rabbits as compared to control (PHF, 3.6+/-1.3; Sham, 4.4+/-0.6 mN/mm2). Rapid cooling contractures (RCCs) were unchanged indicating preserved SR Ca2+ load at this frequency. In Sham, isometric twitch force increased with rising frequencies to 29.0+/-2.8 mN/mm2 at 3.0 Hz (p < 0.05) as compared to 0.25 Hz. RCCs showed a parallel increase by 186+/-47% (p < 0.01). In PHF, frequency-dependent increase in force (15.8+/-4.7 mN/mm2 at 3.0 Hz) and RCCs (increase by 70+/-40%) were significantly blunted. Thus, in PHF in rabbits SR Ca2+ load is preserved at low frequencies despite decreased SR Ca2+-ATPase expression. This may result from [Na+]i-dependent changes in Na+/Ca2+ exchanger activity.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
1388-9842
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pubmed:author |
pubmed-author:ChristiansClausC,
pubmed-author:HasenfussGerdG,
pubmed-author:KohlhaasMichaelM,
pubmed-author:MaierLars SLS,
pubmed-author:NebendahlKlausK,
pubmed-author:SchillingerWolfgangW,
pubmed-author:SchmidtAlbrecht GAG,
pubmed-author:SchunckOrtwinO,
pubmed-author:SossallaSamuelS,
pubmed-author:TeucherNilsN,
pubmed-author:Van NguyenPhucP,
pubmed-author:ZeitzOliverO
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pubmed:issnType |
Print
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pubmed:volume |
8
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
673-80
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pubmed:dateRevised |
2011-6-8
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pubmed:meshHeading |
pubmed-meshheading:16540370-Animals,
pubmed-meshheading:16540370-Calcium-Transporting ATPases,
pubmed-meshheading:16540370-Disease Models, Animal,
pubmed-meshheading:16540370-Electric Stimulation,
pubmed-meshheading:16540370-Heart Failure,
pubmed-meshheading:16540370-Muscle Cells,
pubmed-meshheading:16540370-Rabbits,
pubmed-meshheading:16540370-Sarcoplasmic Reticulum,
pubmed-meshheading:16540370-Sodium,
pubmed-meshheading:16540370-Sodium-Calcium Exchanger
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pubmed:year |
2006
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pubmed:articleTitle |
High intracellular Na+ preserves myocardial function at low heart rates in isolated myocardium from failing hearts.
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pubmed:affiliation |
Georg-August-Universität Göttingen, Herzzentrum, Kardiologie und Pneumologie, Robert-Koch-Str. 40, 37099 Göttingen, Germany. schiwolf@med.uni-goettingen.de
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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