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   <subfield code="a">T3 and T4 decrease ROS levels and increase endothelial nitric oxide synthase expression in the myocardium of infarcted rats</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Alexandre de Castro, Angela Tavares, Rafael Fernandes, Cristina Campos, Adriana Conzatti, Rafaela Siqueira, Tânia Fernandes, Paulo Schenkel, Carmem Sartório, Susana Llesuy, Adriane Belló-Klein, Alex da Rosa Araujo]</subfield>
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   <subfield code="a">Myocardial infarction leads to a reduction in nitric oxide (NO) bioavailability and an increase in reactive oxygen species (ROS) levels. This scenario has been shown to be detrimental to the heart. Recent studies have shown that thyroid hormone (TH) administration presents positive effects after ischaemic injury. Based on this, the aim of this study was to evaluate the effect of TH on NO bioavailability as well as on endothelial nitric oxide synthase (eNOS) expression after myocardial infarction. Male Wistar rats were divided into three groups: Sham-operated (SHAM), infarcted (AMI) and infarcted+TH (AMIT). During 26days, the AMIT group received T3 and T4 (2 and 8µg/100g/day, respectively) by gavage, while SHAM and AMI rats received saline. After this, the rats underwent echocardiographic analysis were sacrificed, and the left ventricle was collected for biochemical and molecular analysis. Statistical analysis: one-way ANOVA with Student-Newman-Keuls post test. AMI rats presented a 38% increase in ROS levels. TH administration prevented these alterations in AMIT rats. The AMIT group presented an increase in eNOS expression, in NOS activity and in nitrite levels. TH administration also increased PGC-1α expression in the AMIT group. In conclusion, TH effects seem to involve a modulation of eNOS expression and an improvement in NO bioavailability in the infarcted heart.</subfield>
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   <subfield code="a">Springer Science+Business Media New York, 2015</subfield>
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   <subfield code="a">Heart failure</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Thyroid hormones</subfield>
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   <subfield code="a">Nitric oxide</subfield>
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   <subfield code="a">de Castro</subfield>
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   <subfield code="u">Laboratório de Fisiologia Cardiovascular, Departamento de Fisiologia, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Rua Sarmento Leite 500, sala 01, CEP 90050170, Porto Alegre, RS, Brazil</subfield>
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   <subfield code="u">Laboratório de Fisiologia Cardiovascular, Departamento de Fisiologia, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Rua Sarmento Leite 500, sala 01, CEP 90050170, Porto Alegre, RS, Brazil</subfield>
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   <subfield code="t">Molecular and Cellular Biochemistry</subfield>
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   <subfield code="a">Metadata rights reserved</subfield>
   <subfield code="b">Springer special CC-BY-NC licence</subfield>
   <subfield code="2">nationallicence</subfield>
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