Effects of increased myocardial tissue concentration of myristic, palmitic and palmitoleic acids on the course of cardiac atrophy of the failing heart unloaded by heterotopic transplantation
Jazyk angličtina Země Česko Médium print-electronic
Typ dokumentu časopisecké články
PubMed
29137478
DOI
10.33549/physiolres.933637
PII: 933637
Knihovny.cz E-zdroje
- MeSH
- heterotopická transplantace metody MeSH
- kardiomyocyty metabolismus MeSH
- krysa rodu Rattus MeSH
- kyselina myristová metabolismus MeSH
- kyselina palmitová metabolismus MeSH
- kyseliny mastné mononenasycené metabolismus MeSH
- myokard metabolismus patologie MeSH
- potkani inbrední LEW MeSH
- srdeční selhání metabolismus chirurgie MeSH
- transplantace srdce metody MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- kyselina myristová MeSH
- kyselina palmitová MeSH
- kyseliny mastné mononenasycené MeSH
- palmitoleic acid MeSH Prohlížeč
The present experiments were performed to evaluate if increased heart tissue concentration of fatty acids, specifically myristic, palmitic and palmitoleic acids that are believed to promote physiological heart growth, can attenuate the progression of unloading-induced cardiac atrophy in rats with healthy and failing hearts. Heterotopic abdominal heart transplantation (HT(x)) was used as a model for heart unloading. Cardiac atrophy was assessed from the ratio of the native- to-transplanted heart weight (HW). The degree of cardiac atrophy after HT(x) was determined on days 7, 14, 21 and 28 after HT(x) in recipients of either healthy or failing hearts. HT(x) of healthy hearts resulted in 23+/-3, 46+/-3, 48+/-4 and 46+/-4 % HW loss at the four time-points. HT(x) of the failing heart resulted in even greater HW losses, of 46+/-4, 58+/-3, 66+/-2 and 68+/-4 %, respectively (P<0.05). Activation of "fetal gene cardiac program" (e.g. beta myosin heavy chain gene expression) and "genes reflecting cardiac remodeling" (e.g. atrial natriuretic peptide gene expression) after HT(x) was greater in failing than in healthy hearts (P<0.05 each time). Exposure to isocaloric high sugar diet caused significant increases in fatty acid concentrations in healthy and in failing hearts. However, these increases were not associated with any change in the course of cardiac atrophy, similarly in healthy and post-HT(x) failing hearts. We conclude that increasing heart tissue concentrations of the fatty acids allegedly involved in heart growth does not attenuate the unloading-induced cardiac atrophy.
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