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dc.contributor.authorJohnsen, Anne Berit
dc.contributor.authorHøydal, Morten Andre
dc.contributor.authorRøsbjørgen, Ragnhild
dc.contributor.authorStølen, Tomas
dc.contributor.authorWisløff, Ulrik
dc.identifier.citationPLoS ONE 2013, 8(6:e66288)nb_NO
dc.description.abstractBackground: There is limited knowledge about atrial myocyte Ca2+ handling in the failing hearts. The aim of this study was to examine atrial myocyte contractile function and Ca2+ handling in rats with post-infarction heart failure (HF) and to examine whether aerobic interval training could reverse a potential dysfunction. Methods and results: Post-infarction HF was induced in Sprague Dawley rats by ligation of the left descending coronary artery. Atrial myocyte shortening was depressed (p<0.01) and time to relaxation was prolonged (p<0.01) in sedentary HF-rats compared to healthy controls. This was associated with decreased Ca2+ amplitude, decreased SR Ca2+ content, and slower Ca2+ transient decay. Atrial myocytes from HF-rats had reduced sarcoplasmic reticulum Ca2+ ATPase activity, increased Na+/Ca2+-exchanger activity and increased diastolic Ca2+ leak through ryanodine receptors. High intensity aerobic interval training in HF-rats restored atrial myocyte contractile function and reversed changes in atrial Ca2+ handling in HF. Conclusion: Post infarction HF in rats causes profound impairment in atrial myocyte contractile function and Ca2+ handling. The observed dysfunction in atrial myocytes was partly reversed after aerobic interval training.nb_NO
dc.publisherPublic Library of Sciencenb_NO
dc.rightsNavngivelse 3.0 Norge*
dc.titleAerobic interval training partly reverse contractile dysfunction and impaired Ca2+ handling in atrial myocytes from rats with post infarction heart failurenb_NO
dc.typeJournal articlenb_NO
dc.typePeer reviewednb_NO
dc.source.journalPLoS ONEnb_NO
dc.description.localcode© 2013 Johnsen et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.nb_NO

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Navngivelse 3.0 Norge
Except where otherwise noted, this item's license is described as Navngivelse 3.0 Norge