ArticleChonnam medical journal2018
Effects of Ivabradine on Left Ventricular Systolic Function and Cardiac Fibrosis in Rat Myocardial Ischemia-Reperfusion Model.
Article in Chonnam medical journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Heart rate management using ivabradine in acute myocardial infarction: a propensity score-matched single-center study.Scientific reports · 2025Article
- Therapeutic Use and Molecular Aspects of Ivabradine in Cardiac Remodeling: A Review.International journal of molecular sciences · 2023Review
- TRPV1 Contributes to Modulate the Nitric Oxide Pathway and Oxidative Stress in the Isolated and Perfused Rat Heart during Ischemia and Reperfusion.Molecules (Basel, Switzerland) · 2022Article
- Crosstalk between the activated Slit2-Robo1 pathway and TGF-β1 signalling promotes cardiac fibrosis.ESC heart failure · 2021Article
- Diosmetin exerts cardioprotective effect on myocardial ischaemia injury in neonatal rats by decreasing oxidative stress and myocardial apoptosis.Clinical and experimental pharmacology & physiology · 2020Article
- Etomidate alleviates cardiac dysfunction, fibrosis and oxidative stress in rats with myocardial ischemic reperfusion injury.Annals of translational medicine · 2020Article
- Evidence for Effective Inhibitory Actions on Hyperpolarization-Activated Cation Current Caused byMolecules (Basel, Switzerland) · 2019Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We evaluated the effects of Ivabradine on left ventricle (LV) ejection fraction (EF) and LV infarcted tissue in the rat myocardial ischemia-reperfusion model. Twenty rats were randomly assigned to group 1 (ischemia-reperfusion, no treatment, n=10) and group 2 (ischemia-reperfusion + Ivabradine 10 mg/kg, n=10). Ivabradine was administered for 28 days. Echocardiography was performed at 7 days and at 28 days after the induction of ischemia-reperfusion injury. Cardiac fibrosis induced by ischemia-reperfusion injury was evaluated by Masson's trichrome staining. The infarct size was quantified using the Image J program. At the 28-day follow-up, LVEF was significantly higher (36.02±6.16% vs. 45.72±2.62%, p<0.001) and fractional shortening was significantly higher (15.23±2.84% vs. 20.13±1.38%, p<0.001) in group 2 than group 1. Delta (28 day minus 7 day) EF was significantly higher in group 2 than group 1 (-4.36±3.49% vs. 4.31±5.63%, p<0.001). Also, heart rate (beats/min) was significantly lower in group 2 than group 1 (251.67±25.19 vs. 199.29±31.33, p=0.025). Group 2 had a smaller infarct size (40.70±8.94% vs. 30.19±5.89%, p<0.01) than group 1 at 28-day follow-up. Oral administration of Ivabradine could improve LV systolic function and reduce infarcted tissue area in rat myocardial ischemia-reperfusion model.
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