Beneficial effects of intravenous iron therapy in a rat model of heart failure with preserved systemic iron status but depleted intracellular cardiac stores

Autor: Michał Mączewski, Przemysław Leszek, Halina Polkowska-Motrenko, Urszula Mackiewicz, Marta Kępska, Aleksandra Paterek, Ewelina Chajduk, Joanna Kołodziejczyk, Barbara Sochanowicz, Marcin Kruszewski
Rok vydání: 2018
Předmět:
0301 basic medicine
Male
Intracellular Space
Myocardial Infarction
030204 cardiovascular system & hematology
medicine.disease_cause
0302 clinical medicine
Ferric Carboxymaltose
Myocytes
Cardiac
Systemic Iron Status
Multidisciplinary
Ejection fraction
biology
Iron deficiency
Liver
Injections
Intravenous
Intravenous Iron Supplementation
Medicine
Myocardial Iron Content
medicine.medical_specialty
Anemia
Science
Heart Ventricles
Iron
Article
Sarcoplasmic Reticulum (SR) Ca2+-ATPase (SERCA)
Superoxide dismutase
03 medical and health sciences
Internal medicine
medicine
Animals
Calcium Signaling
Rats
Wistar
Heart Failure
Inflammation
Transferrin saturation
business.industry
Myocardium
Hemodynamics
medicine.disease
Ferritin
Disease Models
Animal
Oxidative Stress
030104 developmental biology
Endocrinology
Heart failure
biology.protein
business
Oxidative stress
Biomarkers
Zdroj: Scientific Reports
Scientific Reports, Vol 8, Iss 1, Pp 1-15 (2018)
ISSN: 2045-2322
Popis: Iron deficiency (ID) commonly occurs in chronic heart failure (HF) and is associated with poor prognosis. Neither its causes nor pathophysiological significance are clearly understood. We aimed to assess iron status and the effect of iron supplementation in the rat model of post-myocardial infarction (MI) HF. Four weeks after induction of MI to induce HF or sham surgery, rats received intravenous iron (ferric carboxymaltose) or saline, 4 doses in 1-week intervals. HF alone did not cause anemia, systemic or myocardial ID, but reduced myocardial ferritin, suggesting depleted cardiomyocyte iron stores. Iron therapy increased serum Fe, ferritin and transferrin saturation as well as cardiac and hepatic iron content in HF rats, but did not increase myocardial ferritin. This was accompanied by: (1) better preservation of left ventricular (LV) ejection fraction and smaller LV dilation, (2) preservation of function of Ca2+ handling proteins in LV cardiomyocytes and (3) reduced level of inflammatory marker, CRP. Furthermore, iron supplementation did not potentiate oxidative stress or have toxic effects on cardiomyocyte function, but increased activity of antioxidant defenses (cardiac superoxide dismutase). Despite lack of systemic or myocardial ID we found evidence of depleted cardiomyocyte iron stores in the rat model of HF. Furthermore we observed positive effect of iron supplementation and confirmed safety of iron supplementation in this setting.
Databáze: OpenAIRE
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