Diabetic hyperglycemia attenuates sympathetic dysfunction and oxidative stress after myocardial infarction in rats

Autores
Malfitano, Christiane; Andrade Barboza, Catarina de; Mostarda, Cristiano; Palma, Renata Kelly da; Santos, Camila Paixão dos; Rodrigues, Bruno; Ferreira Freitas, Sarah Cristina; Belló Klein, Adriane; Llesuy, Susana Francisca; Irigoyen, Maria Cláudia; De Angelis, Kátia
Año de publicación
2014
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Background: Previous research has demonstrated that hyperglycemia may protect the heart against ischemic injury. The aim of the present study was to investigate the association between hyperglycemia and myocardial infarction on cardiovascular autonomic modulation and cardiac oxidative stress profile in rats. Male Wistar rats were divided into: control (C), diabetic (D), myocardial infarcted (MI) and diabetic infarcted rats (DMI). Methods: Diabetes was induced by streptozotocin (STZ, 50 mg/Kg) at the beginning of the protocol and MI was induced by left coronary occlusion 15 days after STZ. Thirty days after streptozocin-induced diabetes, cardiovascular autonomic modulation was evaluated by spectral analysis, and oxidative stress profile was determined by antioxidant enzyme activities and superoxide anion, together with protein carbonylation and redox balance of glutathione (GSH/GSSG). Results: The diabetic and infarcted groups showed decreased heart rate variability and vagal modulation (p < 0.05); however, sympathetic modulation decreased only in diabetic groups (p < 0.05). Sympatho/vagal balance and vascular sympathetic modulation were increased only in the MI group (p < 0.05). Diabetes promoted an increase in catalase concentration (p < 0.05). Glutathione peroxidase activity was increased only in DMI when compared to the other groups (p < 0.05). Superoxide anion and protein carbonylation were increased only in MI group (p < 0.05). Cardiac redox balance, as evaluated by GSH/GSSG, was lower in the MI group (p < 0.05). Conclusions: These data suggest that hyperglycemia promotes compensatory mechanisms that may offer protection against ischemia, as demonstrated by increased antioxidants, decreased pro-oxidants and protein damage, possibly related to the improvements in both redox balance and sympathetic modulation to the heart.
Fil: Malfitano, Christiane. Universidade Nove de Julho ; Brasil
Fil: Andrade Barboza, Catarina de. Universidade São Judas Tadeu; Brasil
Fil: Mostarda, Cristiano. Universidade Federal do Maranhão ; Brasil. Universidade de Sao Paulo; Brasil
Fil: Palma, Renata Kelly da. Universidade Nove de Julho ; Brasil
Fil: Santos, Camila Paixão dos. Universidade Nove de Julho ; Brasil
Fil: Rodrigues, Bruno. Universidade São Judas Tadeu; Brasil
Fil: Ferreira Freitas, Sarah Cristina. Universidade Nove de Julho ; Brasil
Fil: Belló Klein, Adriane. Universidade Nove de Julho ; Brasil. Universidade Federal do Rio Grande do Sul; Brasil
Fil: Llesuy, Susana Francisca. Universidade Nove de Julho ; Brasil. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Bioquímica y Medicina Molecular; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Analítica y Fisicoquímica. Cátedra de Química General e Inorgánica; Argentina
Fil: Irigoyen, Maria Cláudia. Universidade de Sao Paulo; Brasil
Fil: De Angelis, Kátia. Universidade Nove de Julho ; Brasil
Materia
Autonomic modulation
Oxidative stress
Diabetic hyperglycemia
Myocardial infarction
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/30795
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/30795
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Diabetic hyperglycemia attenuates sympathetic dysfunction and oxidative stress after myocardial infarction in ratsMalfitano, ChristianeAndrade Barboza, Catarina deMostarda, CristianoPalma, Renata Kelly daSantos, Camila Paixão dosRodrigues, BrunoFerreira Freitas, Sarah CristinaBelló Klein, AdrianeLlesuy, Susana FranciscaIrigoyen, Maria CláudiaDe Angelis, KátiaAutonomic modulationOxidative stressDiabetic hyperglycemiaMyocardial infarctionhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Background: Previous research has demonstrated that hyperglycemia may protect the heart against ischemic injury. The aim of the present study was to investigate the association between hyperglycemia and myocardial infarction on cardiovascular autonomic modulation and cardiac oxidative stress profile in rats. Male Wistar rats were divided into: control (C), diabetic (D), myocardial infarcted (MI) and diabetic infarcted rats (DMI). Methods: Diabetes was induced by streptozotocin (STZ, 50 mg/Kg) at the beginning of the protocol and MI was induced by left coronary occlusion 15 days after STZ. Thirty days after streptozocin-induced diabetes, cardiovascular autonomic modulation was evaluated by spectral analysis, and oxidative stress profile was determined by antioxidant enzyme activities and superoxide anion, together with protein carbonylation and redox balance of glutathione (GSH/GSSG). Results: The diabetic and infarcted groups showed decreased heart rate variability and vagal modulation (p < 0.05); however, sympathetic modulation decreased only in diabetic groups (p < 0.05). Sympatho/vagal balance and vascular sympathetic modulation were increased only in the MI group (p < 0.05). Diabetes promoted an increase in catalase concentration (p < 0.05). Glutathione peroxidase activity was increased only in DMI when compared to the other groups (p < 0.05). Superoxide anion and protein carbonylation were increased only in MI group (p < 0.05). Cardiac redox balance, as evaluated by GSH/GSSG, was lower in the MI group (p < 0.05). Conclusions: These data suggest that hyperglycemia promotes compensatory mechanisms that may offer protection against ischemia, as demonstrated by increased antioxidants, decreased pro-oxidants and protein damage, possibly related to the improvements in both redox balance and sympathetic modulation to the heart.Fil: Malfitano, Christiane. Universidade Nove de Julho ; BrasilFil: Andrade Barboza, Catarina de. Universidade São Judas Tadeu; BrasilFil: Mostarda, Cristiano. Universidade Federal do Maranhão ; Brasil. Universidade de Sao Paulo; BrasilFil: Palma, Renata Kelly da. Universidade Nove de Julho ; BrasilFil: Santos, Camila Paixão dos. Universidade Nove de Julho ; BrasilFil: Rodrigues, Bruno. Universidade São Judas Tadeu; BrasilFil: Ferreira Freitas, Sarah Cristina. Universidade Nove de Julho ; BrasilFil: Belló Klein, Adriane. Universidade Nove de Julho ; Brasil. Universidade Federal do Rio Grande do Sul; BrasilFil: Llesuy, Susana Francisca. Universidade Nove de Julho ; Brasil. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Bioquímica y Medicina Molecular; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Analítica y Fisicoquímica. Cátedra de Química General e Inorgánica; ArgentinaFil: Irigoyen, Maria Cláudia. Universidade de Sao Paulo; BrasilFil: De Angelis, Kátia. Universidade Nove de Julho ; BrasilBioMed Central2014-10info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/30795De Angelis, Kátia; Irigoyen, Maria Cláudia; Llesuy, Susana Francisca; Belló Klein, Adriane; Ferreira Freitas, Sarah Cristina; Rodrigues, Bruno; et al.; Diabetic hyperglycemia attenuates sympathetic dysfunction and oxidative stress after myocardial infarction in rats; BioMed Central; Cardiovascular Diabetology; 13; 131; 10-2014; 1-91475-2840CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4198704/info:eu-repo/semantics/altIdentifier/doi/10.1186/s12933-014-0131-xinfo:eu-repo/semantics/altIdentifier/url/https://cardiab.biomedcentral.com/articles/10.1186/s12933-014-0131-xinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-10T13:16:24Zoai:ri.conicet.gov.ar:11336/30795instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-10 13:16:24.476CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Diabetic hyperglycemia attenuates sympathetic dysfunction and oxidative stress after myocardial infarction in rats
title Diabetic hyperglycemia attenuates sympathetic dysfunction and oxidative stress after myocardial infarction in rats
spellingShingle Diabetic hyperglycemia attenuates sympathetic dysfunction and oxidative stress after myocardial infarction in rats
Malfitano, Christiane
Autonomic modulation
Oxidative stress
Diabetic hyperglycemia
Myocardial infarction
title_short Diabetic hyperglycemia attenuates sympathetic dysfunction and oxidative stress after myocardial infarction in rats
title_full Diabetic hyperglycemia attenuates sympathetic dysfunction and oxidative stress after myocardial infarction in rats
title_fullStr Diabetic hyperglycemia attenuates sympathetic dysfunction and oxidative stress after myocardial infarction in rats
title_full_unstemmed Diabetic hyperglycemia attenuates sympathetic dysfunction and oxidative stress after myocardial infarction in rats
title_sort Diabetic hyperglycemia attenuates sympathetic dysfunction and oxidative stress after myocardial infarction in rats
dc.creator.none.fl_str_mv Malfitano, Christiane
Andrade Barboza, Catarina de
Mostarda, Cristiano
Palma, Renata Kelly da
Santos, Camila Paixão dos
Rodrigues, Bruno
Ferreira Freitas, Sarah Cristina
Belló Klein, Adriane
Llesuy, Susana Francisca
Irigoyen, Maria Cláudia
De Angelis, Kátia
author Malfitano, Christiane
author_facet Malfitano, Christiane
Andrade Barboza, Catarina de
Mostarda, Cristiano
Palma, Renata Kelly da
Santos, Camila Paixão dos
Rodrigues, Bruno
Ferreira Freitas, Sarah Cristina
Belló Klein, Adriane
Llesuy, Susana Francisca
Irigoyen, Maria Cláudia
De Angelis, Kátia
author_role author
author2 Andrade Barboza, Catarina de
Mostarda, Cristiano
Palma, Renata Kelly da
Santos, Camila Paixão dos
Rodrigues, Bruno
Ferreira Freitas, Sarah Cristina
Belló Klein, Adriane
Llesuy, Susana Francisca
Irigoyen, Maria Cláudia
De Angelis, Kátia
author2_role author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Autonomic modulation
Oxidative stress
Diabetic hyperglycemia
Myocardial infarction
topic Autonomic modulation
Oxidative stress
Diabetic hyperglycemia
Myocardial infarction
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Background: Previous research has demonstrated that hyperglycemia may protect the heart against ischemic injury. The aim of the present study was to investigate the association between hyperglycemia and myocardial infarction on cardiovascular autonomic modulation and cardiac oxidative stress profile in rats. Male Wistar rats were divided into: control (C), diabetic (D), myocardial infarcted (MI) and diabetic infarcted rats (DMI). Methods: Diabetes was induced by streptozotocin (STZ, 50 mg/Kg) at the beginning of the protocol and MI was induced by left coronary occlusion 15 days after STZ. Thirty days after streptozocin-induced diabetes, cardiovascular autonomic modulation was evaluated by spectral analysis, and oxidative stress profile was determined by antioxidant enzyme activities and superoxide anion, together with protein carbonylation and redox balance of glutathione (GSH/GSSG). Results: The diabetic and infarcted groups showed decreased heart rate variability and vagal modulation (p < 0.05); however, sympathetic modulation decreased only in diabetic groups (p < 0.05). Sympatho/vagal balance and vascular sympathetic modulation were increased only in the MI group (p < 0.05). Diabetes promoted an increase in catalase concentration (p < 0.05). Glutathione peroxidase activity was increased only in DMI when compared to the other groups (p < 0.05). Superoxide anion and protein carbonylation were increased only in MI group (p < 0.05). Cardiac redox balance, as evaluated by GSH/GSSG, was lower in the MI group (p < 0.05). Conclusions: These data suggest that hyperglycemia promotes compensatory mechanisms that may offer protection against ischemia, as demonstrated by increased antioxidants, decreased pro-oxidants and protein damage, possibly related to the improvements in both redox balance and sympathetic modulation to the heart.
Fil: Malfitano, Christiane. Universidade Nove de Julho ; Brasil
Fil: Andrade Barboza, Catarina de. Universidade São Judas Tadeu; Brasil
Fil: Mostarda, Cristiano. Universidade Federal do Maranhão ; Brasil. Universidade de Sao Paulo; Brasil
Fil: Palma, Renata Kelly da. Universidade Nove de Julho ; Brasil
Fil: Santos, Camila Paixão dos. Universidade Nove de Julho ; Brasil
Fil: Rodrigues, Bruno. Universidade São Judas Tadeu; Brasil
Fil: Ferreira Freitas, Sarah Cristina. Universidade Nove de Julho ; Brasil
Fil: Belló Klein, Adriane. Universidade Nove de Julho ; Brasil. Universidade Federal do Rio Grande do Sul; Brasil
Fil: Llesuy, Susana Francisca. Universidade Nove de Julho ; Brasil. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Bioquímica y Medicina Molecular; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Analítica y Fisicoquímica. Cátedra de Química General e Inorgánica; Argentina
Fil: Irigoyen, Maria Cláudia. Universidade de Sao Paulo; Brasil
Fil: De Angelis, Kátia. Universidade Nove de Julho ; Brasil
description Background: Previous research has demonstrated that hyperglycemia may protect the heart against ischemic injury. The aim of the present study was to investigate the association between hyperglycemia and myocardial infarction on cardiovascular autonomic modulation and cardiac oxidative stress profile in rats. Male Wistar rats were divided into: control (C), diabetic (D), myocardial infarcted (MI) and diabetic infarcted rats (DMI). Methods: Diabetes was induced by streptozotocin (STZ, 50 mg/Kg) at the beginning of the protocol and MI was induced by left coronary occlusion 15 days after STZ. Thirty days after streptozocin-induced diabetes, cardiovascular autonomic modulation was evaluated by spectral analysis, and oxidative stress profile was determined by antioxidant enzyme activities and superoxide anion, together with protein carbonylation and redox balance of glutathione (GSH/GSSG). Results: The diabetic and infarcted groups showed decreased heart rate variability and vagal modulation (p < 0.05); however, sympathetic modulation decreased only in diabetic groups (p < 0.05). Sympatho/vagal balance and vascular sympathetic modulation were increased only in the MI group (p < 0.05). Diabetes promoted an increase in catalase concentration (p < 0.05). Glutathione peroxidase activity was increased only in DMI when compared to the other groups (p < 0.05). Superoxide anion and protein carbonylation were increased only in MI group (p < 0.05). Cardiac redox balance, as evaluated by GSH/GSSG, was lower in the MI group (p < 0.05). Conclusions: These data suggest that hyperglycemia promotes compensatory mechanisms that may offer protection against ischemia, as demonstrated by increased antioxidants, decreased pro-oxidants and protein damage, possibly related to the improvements in both redox balance and sympathetic modulation to the heart.
publishDate 2014
dc.date.none.fl_str_mv 2014-10
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/30795
De Angelis, Kátia; Irigoyen, Maria Cláudia; Llesuy, Susana Francisca; Belló Klein, Adriane; Ferreira Freitas, Sarah Cristina; Rodrigues, Bruno; et al.; Diabetic hyperglycemia attenuates sympathetic dysfunction and oxidative stress after myocardial infarction in rats; BioMed Central; Cardiovascular Diabetology; 13; 131; 10-2014; 1-9
1475-2840
CONICET Digital
CONICET
url http://hdl.handle.net/11336/30795
identifier_str_mv De Angelis, Kátia; Irigoyen, Maria Cláudia; Llesuy, Susana Francisca; Belló Klein, Adriane; Ferreira Freitas, Sarah Cristina; Rodrigues, Bruno; et al.; Diabetic hyperglycemia attenuates sympathetic dysfunction and oxidative stress after myocardial infarction in rats; BioMed Central; Cardiovascular Diabetology; 13; 131; 10-2014; 1-9
1475-2840
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4198704/
info:eu-repo/semantics/altIdentifier/doi/10.1186/s12933-014-0131-x
info:eu-repo/semantics/altIdentifier/url/https://cardiab.biomedcentral.com/articles/10.1186/s12933-014-0131-x
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv BioMed Central
publisher.none.fl_str_mv BioMed Central
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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score 12.993085

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