Early loss of cardiac function in acute myocardial infarction is associated with redox imbalance
- Autores
- Vicente Tavares, Angela María; da Rosa Araujo, Alex Sande; Llesuy, Susana Francisca; Khaper, Neelam; Rohde, Luis Eduardo; Clausell, Nadine; Bello Klein, Adriane
- Año de publicación
- 2012
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- BACKGROUND: The loss of viable myocardium subsequent to myocardial infarction (MI) impairs cardiac function, and oxidative stress is considered to be critical in this process. OBJECTIVES: To assess cardiac function and correlate it with oxidative stress and antioxidant levels in cardiac tissue at 48 h post-MI. METHODS: Adult male Wistar rats (n=6 per group) with a mean (± SD) weight of 229±24 g were randomly assigned to either an infarcted group or a control group. MI was induced by occlusion of the left coronary artery. Cardiac function was evaluated by measuring left ventricular (LV) ejection fraction, LV fractional shortening, cardiac output, myocardial performance index and the peak early diastolic velocity/peak atrial velocity ratio using echocardiography. The myocardial oxidative stress profile was assessed by measuring the reduced glutathione/oxidized glutathione ratio, H2O2 levels, peroxiredoxin-6 protein levels and activity levels of superoxide dismutase, catalase and glutathione peroxidase. Lipid peroxidation was quantified using chemiluminescence, and protein oxidation was determined by measuring protein carbonyl levels. RESULTS: LV ejection fraction and LV fractional shortening were lower in the infarcted group compared with the sham group, whereas the peak early diastolic velocity/peak atrial velocity ratio and myocardial performance index were significantly increased, indicating systolic dysfunction. Lipid peroxidation, protein carbonyls and superoxide dismutase and catalase activity levels did not differ between the groups. Peroxyredoxin-6 levels were increased in the infarcted group, while H2O2 levels were reduced. The reduced glutathione/oxidized glutathione ratio and the glutathione peroxidase activity were reduced in the infarcted group compared with control. DISCUSSION AND CONCLUSION: These data suggest that MI-induced cardiac dysfunction and impaired redox balance may be associated with the activation of counter-regulatory responses to maintain reduced H2O2 concentrations and, thereby, prevent further oxidative damage at this early time point.
Fil: Vicente Tavares, Angela María. Universidade Federal do Rio Grande do Sul. Instituto de Ciências Básicas da Saude; Brasil
Fil: da Rosa Araujo, Alex Sande. Universidade Federal do Rio Grande do Sul; Brasil
Fil: Llesuy, Susana Francisca. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. 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: Khaper, Neelam. Universidade Federal do Rio Grande do Sul. Instituto de Ciências Básicas da Saude; Brasil
Fil: Rohde, Luis Eduardo. Universidade Federal do Rio Grande do Sul. Instituto de Ciências Básicas da Saude; Brasil
Fil: Clausell, Nadine. Universidade Federal do Rio Grande do Sul. Instituto de Ciências Básicas da Saude; Brasil
Fil: Bello Klein, Adriane. Universidade Federal do Rio Grande do Sul; Brasil - Materia
-
Acute myocardial infarction,
Cardiac function,
Redox imbalance - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
- Repositorio
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/151538
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Early loss of cardiac function in acute myocardial infarction is associated with redox imbalanceVicente Tavares, Angela Maríada Rosa Araujo, Alex SandeLlesuy, Susana FranciscaKhaper, NeelamRohde, Luis EduardoClausell, NadineBello Klein, AdrianeAcute myocardial infarction,Cardiac function,Redox imbalancehttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1BACKGROUND: The loss of viable myocardium subsequent to myocardial infarction (MI) impairs cardiac function, and oxidative stress is considered to be critical in this process. OBJECTIVES: To assess cardiac function and correlate it with oxidative stress and antioxidant levels in cardiac tissue at 48 h post-MI. METHODS: Adult male Wistar rats (n=6 per group) with a mean (± SD) weight of 229±24 g were randomly assigned to either an infarcted group or a control group. MI was induced by occlusion of the left coronary artery. Cardiac function was evaluated by measuring left ventricular (LV) ejection fraction, LV fractional shortening, cardiac output, myocardial performance index and the peak early diastolic velocity/peak atrial velocity ratio using echocardiography. The myocardial oxidative stress profile was assessed by measuring the reduced glutathione/oxidized glutathione ratio, H2O2 levels, peroxiredoxin-6 protein levels and activity levels of superoxide dismutase, catalase and glutathione peroxidase. Lipid peroxidation was quantified using chemiluminescence, and protein oxidation was determined by measuring protein carbonyl levels. RESULTS: LV ejection fraction and LV fractional shortening were lower in the infarcted group compared with the sham group, whereas the peak early diastolic velocity/peak atrial velocity ratio and myocardial performance index were significantly increased, indicating systolic dysfunction. Lipid peroxidation, protein carbonyls and superoxide dismutase and catalase activity levels did not differ between the groups. Peroxyredoxin-6 levels were increased in the infarcted group, while H2O2 levels were reduced. The reduced glutathione/oxidized glutathione ratio and the glutathione peroxidase activity were reduced in the infarcted group compared with control. DISCUSSION AND CONCLUSION: These data suggest that MI-induced cardiac dysfunction and impaired redox balance may be associated with the activation of counter-regulatory responses to maintain reduced H2O2 concentrations and, thereby, prevent further oxidative damage at this early time point.Fil: Vicente Tavares, Angela María. Universidade Federal do Rio Grande do Sul. Instituto de Ciências Básicas da Saude; BrasilFil: da Rosa Araujo, Alex Sande. Universidade Federal do Rio Grande do Sul; BrasilFil: Llesuy, Susana Francisca. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. 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: Khaper, Neelam. Universidade Federal do Rio Grande do Sul. Instituto de Ciências Básicas da Saude; BrasilFil: Rohde, Luis Eduardo. Universidade Federal do Rio Grande do Sul. Instituto de Ciências Básicas da Saude; BrasilFil: Clausell, Nadine. Universidade Federal do Rio Grande do Sul. Instituto de Ciências Básicas da Saude; BrasilFil: Bello Klein, Adriane. Universidade Federal do Rio Grande do Sul; BrasilPulsus Group Inc2012-12info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/151538Vicente Tavares, Angela María; da Rosa Araujo, Alex Sande; Llesuy, Susana Francisca; Khaper, Neelam; Rohde, Luis Eduardo; et al.; Early loss of cardiac function in acute myocardial infarction is associated with redox imbalance; Pulsus Group Inc; Experimental Cardiology; 17; 12-2012; 263-2671205-6626CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3627290/info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:07:11Zoai:ri.conicet.gov.ar:11336/151538instacron: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:34982025-09-03 10:07:11.809CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
dc.title.none.fl_str_mv |
Early loss of cardiac function in acute myocardial infarction is associated with redox imbalance |
title |
Early loss of cardiac function in acute myocardial infarction is associated with redox imbalance |
spellingShingle |
Early loss of cardiac function in acute myocardial infarction is associated with redox imbalance Vicente Tavares, Angela María Acute myocardial infarction, Cardiac function, Redox imbalance |
title_short |
Early loss of cardiac function in acute myocardial infarction is associated with redox imbalance |
title_full |
Early loss of cardiac function in acute myocardial infarction is associated with redox imbalance |
title_fullStr |
Early loss of cardiac function in acute myocardial infarction is associated with redox imbalance |
title_full_unstemmed |
Early loss of cardiac function in acute myocardial infarction is associated with redox imbalance |
title_sort |
Early loss of cardiac function in acute myocardial infarction is associated with redox imbalance |
dc.creator.none.fl_str_mv |
Vicente Tavares, Angela María da Rosa Araujo, Alex Sande Llesuy, Susana Francisca Khaper, Neelam Rohde, Luis Eduardo Clausell, Nadine Bello Klein, Adriane |
author |
Vicente Tavares, Angela María |
author_facet |
Vicente Tavares, Angela María da Rosa Araujo, Alex Sande Llesuy, Susana Francisca Khaper, Neelam Rohde, Luis Eduardo Clausell, Nadine Bello Klein, Adriane |
author_role |
author |
author2 |
da Rosa Araujo, Alex Sande Llesuy, Susana Francisca Khaper, Neelam Rohde, Luis Eduardo Clausell, Nadine Bello Klein, Adriane |
author2_role |
author author author author author author |
dc.subject.none.fl_str_mv |
Acute myocardial infarction, Cardiac function, Redox imbalance |
topic |
Acute myocardial infarction, Cardiac function, Redox imbalance |
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: The loss of viable myocardium subsequent to myocardial infarction (MI) impairs cardiac function, and oxidative stress is considered to be critical in this process. OBJECTIVES: To assess cardiac function and correlate it with oxidative stress and antioxidant levels in cardiac tissue at 48 h post-MI. METHODS: Adult male Wistar rats (n=6 per group) with a mean (± SD) weight of 229±24 g were randomly assigned to either an infarcted group or a control group. MI was induced by occlusion of the left coronary artery. Cardiac function was evaluated by measuring left ventricular (LV) ejection fraction, LV fractional shortening, cardiac output, myocardial performance index and the peak early diastolic velocity/peak atrial velocity ratio using echocardiography. The myocardial oxidative stress profile was assessed by measuring the reduced glutathione/oxidized glutathione ratio, H2O2 levels, peroxiredoxin-6 protein levels and activity levels of superoxide dismutase, catalase and glutathione peroxidase. Lipid peroxidation was quantified using chemiluminescence, and protein oxidation was determined by measuring protein carbonyl levels. RESULTS: LV ejection fraction and LV fractional shortening were lower in the infarcted group compared with the sham group, whereas the peak early diastolic velocity/peak atrial velocity ratio and myocardial performance index were significantly increased, indicating systolic dysfunction. Lipid peroxidation, protein carbonyls and superoxide dismutase and catalase activity levels did not differ between the groups. Peroxyredoxin-6 levels were increased in the infarcted group, while H2O2 levels were reduced. The reduced glutathione/oxidized glutathione ratio and the glutathione peroxidase activity were reduced in the infarcted group compared with control. DISCUSSION AND CONCLUSION: These data suggest that MI-induced cardiac dysfunction and impaired redox balance may be associated with the activation of counter-regulatory responses to maintain reduced H2O2 concentrations and, thereby, prevent further oxidative damage at this early time point. Fil: Vicente Tavares, Angela María. Universidade Federal do Rio Grande do Sul. Instituto de Ciências Básicas da Saude; Brasil Fil: da Rosa Araujo, Alex Sande. Universidade Federal do Rio Grande do Sul; Brasil Fil: Llesuy, Susana Francisca. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. 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: Khaper, Neelam. Universidade Federal do Rio Grande do Sul. Instituto de Ciências Básicas da Saude; Brasil Fil: Rohde, Luis Eduardo. Universidade Federal do Rio Grande do Sul. Instituto de Ciências Básicas da Saude; Brasil Fil: Clausell, Nadine. Universidade Federal do Rio Grande do Sul. Instituto de Ciências Básicas da Saude; Brasil Fil: Bello Klein, Adriane. Universidade Federal do Rio Grande do Sul; Brasil |
description |
BACKGROUND: The loss of viable myocardium subsequent to myocardial infarction (MI) impairs cardiac function, and oxidative stress is considered to be critical in this process. OBJECTIVES: To assess cardiac function and correlate it with oxidative stress and antioxidant levels in cardiac tissue at 48 h post-MI. METHODS: Adult male Wistar rats (n=6 per group) with a mean (± SD) weight of 229±24 g were randomly assigned to either an infarcted group or a control group. MI was induced by occlusion of the left coronary artery. Cardiac function was evaluated by measuring left ventricular (LV) ejection fraction, LV fractional shortening, cardiac output, myocardial performance index and the peak early diastolic velocity/peak atrial velocity ratio using echocardiography. The myocardial oxidative stress profile was assessed by measuring the reduced glutathione/oxidized glutathione ratio, H2O2 levels, peroxiredoxin-6 protein levels and activity levels of superoxide dismutase, catalase and glutathione peroxidase. Lipid peroxidation was quantified using chemiluminescence, and protein oxidation was determined by measuring protein carbonyl levels. RESULTS: LV ejection fraction and LV fractional shortening were lower in the infarcted group compared with the sham group, whereas the peak early diastolic velocity/peak atrial velocity ratio and myocardial performance index were significantly increased, indicating systolic dysfunction. Lipid peroxidation, protein carbonyls and superoxide dismutase and catalase activity levels did not differ between the groups. Peroxyredoxin-6 levels were increased in the infarcted group, while H2O2 levels were reduced. The reduced glutathione/oxidized glutathione ratio and the glutathione peroxidase activity were reduced in the infarcted group compared with control. DISCUSSION AND CONCLUSION: These data suggest that MI-induced cardiac dysfunction and impaired redox balance may be associated with the activation of counter-regulatory responses to maintain reduced H2O2 concentrations and, thereby, prevent further oxidative damage at this early time point. |
publishDate |
2012 |
dc.date.none.fl_str_mv |
2012-12 |
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/11336/151538 Vicente Tavares, Angela María; da Rosa Araujo, Alex Sande; Llesuy, Susana Francisca; Khaper, Neelam; Rohde, Luis Eduardo; et al.; Early loss of cardiac function in acute myocardial infarction is associated with redox imbalance; Pulsus Group Inc; Experimental Cardiology; 17; 12-2012; 263-267 1205-6626 CONICET Digital CONICET |
url |
http://hdl.handle.net/11336/151538 |
identifier_str_mv |
Vicente Tavares, Angela María; da Rosa Araujo, Alex Sande; Llesuy, Susana Francisca; Khaper, Neelam; Rohde, Luis Eduardo; et al.; Early loss of cardiac function in acute myocardial infarction is associated with redox imbalance; Pulsus Group Inc; Experimental Cardiology; 17; 12-2012; 263-267 1205-6626 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/PMC3627290/ |
dc.rights.none.fl_str_mv |
info:eu-repo/semantics/openAccess https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ |
eu_rights_str_mv |
openAccess |
rights_invalid_str_mv |
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ |
dc.format.none.fl_str_mv |
application/pdf application/pdf |
dc.publisher.none.fl_str_mv |
Pulsus Group Inc |
publisher.none.fl_str_mv |
Pulsus Group Inc |
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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1842269993118466048 |
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13.13397 |