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Ivabradine improves survival and attenuates cardiac remodeling in isoproterenol-induced myocardial injury
F. Simko, T. Baka, K. Repova, S. Aziriova, K. Krajcirovicova, L. Paulis, M. Adamcova
Jazyk angličtina Země Velká Británie
Typ dokumentu časopisecké články
Grantová podpora
PROGRES Q40/5
Univerzita Karlova v Praze
1/0035/19
Vedecká Grantová Agentúra MŠVVaŠ SR a SAV
2/0112/19
Vedecká Grantová Agentúra MŠVVaŠ SR a SAV
PubMed
33098700
DOI
10.1111/fcp.12620
Knihovny.cz E-zdroje
- MeSH
- funkce levé komory srdeční účinky léků MeSH
- infarkt myokardu patofyziologie MeSH
- isoprenalin MeSH
- ivabradin aplikace a dávkování farmakologie MeSH
- kardiotonika aplikace a dávkování farmakologie MeSH
- krysa rodu rattus MeSH
- modely nemocí na zvířatech MeSH
- potkani Wistar MeSH
- remodelace komor účinky léků MeSH
- srdeční selhání farmakoterapie MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
This study investigated whether ivabradine, a selective If current inhibitor reducing heart rate (HR), is able to improve survival and prevent left ventricular (LV) remodeling in isoproterenol-induced heart damage. Wistar rats were treated for 6 weeks: controls (n = 10), ivabradine (10 mg/kg/day orally; n = 10), isoproterenol (5 mg/kg/day intraperitoneally; n = 40), and isoproterenol plus ivabradine (n = 40). Isoproterenol increased mortality, induced hypertrophy of both ventricles and LV fibrotic rebuilding, and reduced systolic blood pressure (SBP). Ivabradine significantly increased survival rate (by 120%) and prolonged average survival time (by 20%). Furthermore, ivabradine reduced LV weight and hydroxyproline content in soluble and insoluble collagen fraction, reduced HR and attenuated SBP decline. We conclude that ivabradine improved survival in isoproterenol-damaged hearts.
Citace poskytuje Crossref.org
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