Ivabradine improves survival and attenuates cardiac remodeling in isoproterenol-induced myocardial injury
Language English Country Great Britain, England Media print-electronic
Document type Journal Article
Grant support
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
PubMed Central
PMC8451821
DOI
10.1111/fcp.12620
Knihovny.cz E-resources
- Keywords
- heart hypertrophy, isoproterenol, ivabradine, mortality, remodeling, survival,
- MeSH
- Ventricular Function, Left drug effects MeSH
- Myocardial Infarction physiopathology MeSH
- Isoproterenol MeSH
- Ivabradine administration & dosage pharmacology MeSH
- Cardiotonic Agents administration & dosage pharmacology MeSH
- Rats MeSH
- Disease Models, Animal MeSH
- Rats, Wistar MeSH
- Ventricular Remodeling drug effects MeSH
- Heart Failure drug therapy MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Isoproterenol MeSH
- Ivabradine MeSH
- Cardiotonic Agents 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.
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