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dc.contributor.author
Toblli, Jorge Eduardo
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Cao, Gabriel Fernando
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Rivas, Carlos Francisco
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Giani, Jorge Fernando
dc.contributor.author
Dominici, Fernando Pablo
dc.date.available
2018-04-12T12:49:12Z
dc.date.issued
2016-06
dc.identifier.citation
Toblli, Jorge Eduardo; Cao, Gabriel Fernando; Rivas, Carlos Francisco; Giani, Jorge Fernando; Dominici, Fernando Pablo; Intravenous iron sucrose reverses anemia-induced cardiac remodeling, prevents myocardial fibrosis, and improves cardiac function by attenuating oxidative/nitrosative stress and inflammation; Elsevier Ireland; International Journal of Cardiology; 212; 6-2016; 84-91
dc.identifier.issn
0167-5273
dc.identifier.uri
http://hdl.handle.net/11336/41829
dc.description.abstract
Background: According to recent clinical trial data, correction of iron deficiency with intravenous (i.v.) iron has favorable outcomes on cardiac function. We evaluated whether i.v. iron treatment of anemic rats has favorable effect on the left ventricular (LV) performance and remodeling and the role of oxidative/nitrosative stress and inflammation in the process. Methods: After weaning, Sprague–Dawley rats were fed low iron diet for 16 weeks, after which the treatment group received five weekly doses of i.v. iron sucrose (10 mg Fe/kg body weight). Echocardiography of LV was performed and hematology parameters were assessed before treatment (baseline, day 0) and at the end of the study (day 29). On day 29, rats were sacrificed and extracellular expansion and fibrosis in LV and interventricular septum were evaluated together with oxidative/nitrosative stress, pro-inflammatory, and repair process markers. Results: Although iron sucrose treatment did not fully correct the anemia, it reversed anemia-induced cardiac remodeling as indicated by echocardiographic and tissue Doppler parameters. Treatment with iron sucrose also prevented anemia-induced myocardial fibrosis as indicated by extracellular expansion and fibrosis markers. Anemia-induced inflammation was prevented by iron sucrose as indicated by the levels of proinflammatory (TNF-α, NF-κB65) and repair process markers (HSP27, HSP70). In addition, iron sucrose treatment significantly reduced (p < 0.01) anemia-induced oxidative and nitrosative stress. Conclusion: Intravenous iron sucrose treatment reversed anemia-induced remodeling of LV, prevented myocardial fibrosis, and improved cardiac function by attenuating oxidative/nitrosative stress and inflammation in the heart.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Elsevier Ireland
dc.rights
info:eu-repo/semantics/restrictedAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
dc.subject
Cardiac Function
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Cardiac Remodeling
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Intravenous Iron Sucrose
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Oxidative Stress
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Rat
dc.subject.classification
Patología
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Medicina Básica
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CIENCIAS MÉDICAS Y DE LA SALUD
dc.title
Intravenous iron sucrose reverses anemia-induced cardiac remodeling, prevents myocardial fibrosis, and improves cardiac function by attenuating oxidative/nitrosative stress and inflammation
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2018-04-10T20:29:58Z
dc.journal.volume
212
dc.journal.pagination
84-91
dc.journal.pais
Irlanda
dc.description.fil
Fil: Toblli, Jorge Eduardo. Hospital Aleman. Laboratorio de Medicina Experimental; Argentina. Universidad de Buenos Aires. Facultad de Medicina; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
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Fil: Cao, Gabriel Fernando. Hospital Aleman. Laboratorio de Medicina Experimental; Argentina. Universidad de Buenos Aires. Facultad de Medicina; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
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Fil: Rivas, Carlos Francisco. Hospital Aleman. Laboratorio de Medicina Experimental; Argentina. Universidad de Buenos Aires. Facultad de Medicina; Argentina
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Fil: Giani, Jorge Fernando. Cedars Sinai Medical Center; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
dc.description.fil
Fil: Dominici, Fernando Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina
dc.journal.title
International Journal of Cardiology
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1016/j.ijcard.2016.03.039
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info:eu-repo/semantics/altIdentifier/url/http://www.internationaljournalofcardiology.com/article/S0167-5273(16)30450-8/fulltext
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0167527316304508