O Piruvato Melhora A Energética Mitocondrial Num Modelo Animal Ex-vivo de Isquemia Miocárdica Global
Autor(a) principal: | |
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Data de Publicação: | 2003 |
Outros Autores: | , , , |
Tipo de documento: | Artigo |
Idioma: | por |
Título da fonte: | Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
Texto Completo: | http://hdl.handle.net/10400.4/341 |
Resumo: | Pyruvate is an energy substrate with known cardioprotective activity. We know now that this is due not only to its antioxidant activity, but also to its reduction of intracellular acidosis, modulation of intracytosolic calcium and improvement of cardiomyocyte contractility. However, the role of cardiac mitochondria in such positive effects has only recently begun to be understood and the exact mechanisms of the effect of pyruvate on mitochondria are still largely unknown. Aiming to study the effect of pyruvate on cardiac mitochondrial function during acute ischemia, we used an ex-vivo animal model, perfused in a Langendorff system and then subjected to ischemia in the presence and absence of pyruvate. We evaluated the mitochondrial membrane electrical potential, the respiratory chain O2 consumption (and respiratory control ratio) and the energy charges generated with different energy substrates. We conclude that pyruvate has some effect on the mitochondrial oxidative system (by non-significantly improving the respiratory control ratio), but its main action is on the phosphorylation system, significantly decreasing the time taken to complete a phosphorylation cycle (lag phase) and improving ATP production (increase in energy charge), thus allowing better maintenance of mitochondrial membrane structure, with consequent improvement of the electrical potential after a phosphorylation cycle. These findings have enabled better understanding of the mechanisms behind pyruvate cytoprotection in ischemic cardiomyopathy, clearly highlighting the essential role of cardiac mitochondria in this process. |
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O Piruvato Melhora A Energética Mitocondrial Num Modelo Animal Ex-vivo de Isquemia Miocárdica GlobalPyruvate improves mitochondrial bioenergetics in an ex-vivo animal model of myocardial ischemiaMitocôndrias CardiacasPiruvatoPyruvate is an energy substrate with known cardioprotective activity. We know now that this is due not only to its antioxidant activity, but also to its reduction of intracellular acidosis, modulation of intracytosolic calcium and improvement of cardiomyocyte contractility. However, the role of cardiac mitochondria in such positive effects has only recently begun to be understood and the exact mechanisms of the effect of pyruvate on mitochondria are still largely unknown. Aiming to study the effect of pyruvate on cardiac mitochondrial function during acute ischemia, we used an ex-vivo animal model, perfused in a Langendorff system and then subjected to ischemia in the presence and absence of pyruvate. We evaluated the mitochondrial membrane electrical potential, the respiratory chain O2 consumption (and respiratory control ratio) and the energy charges generated with different energy substrates. We conclude that pyruvate has some effect on the mitochondrial oxidative system (by non-significantly improving the respiratory control ratio), but its main action is on the phosphorylation system, significantly decreasing the time taken to complete a phosphorylation cycle (lag phase) and improving ATP production (increase in energy charge), thus allowing better maintenance of mitochondrial membrane structure, with consequent improvement of the electrical potential after a phosphorylation cycle. These findings have enabled better understanding of the mechanisms behind pyruvate cytoprotection in ischemic cardiomyopathy, clearly highlighting the essential role of cardiac mitochondria in this process.Sociedade Portuguesa de CardiologiaRIHUCMonteiro, PDuarte, AIMoreno, AJGonçalves, LProvidência, LA2008-12-12T15:17:55Z20032003-01-01T00:00:00Zinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleapplication/pdfhttp://hdl.handle.net/10400.4/341porRev Port Cardiol. 2003 Jan;22(1):79-88info:eu-repo/semantics/openAccessreponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãoinstacron:RCAAP2023-07-11T14:21:30Zoai:rihuc.huc.min-saude.pt:10400.4/341Portal AgregadorONGhttps://www.rcaap.pt/oai/openaireopendoar:71602024-03-19T18:03:09.025227Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãofalse |
dc.title.none.fl_str_mv |
O Piruvato Melhora A Energética Mitocondrial Num Modelo Animal Ex-vivo de Isquemia Miocárdica Global Pyruvate improves mitochondrial bioenergetics in an ex-vivo animal model of myocardial ischemia |
title |
O Piruvato Melhora A Energética Mitocondrial Num Modelo Animal Ex-vivo de Isquemia Miocárdica Global |
spellingShingle |
O Piruvato Melhora A Energética Mitocondrial Num Modelo Animal Ex-vivo de Isquemia Miocárdica Global Monteiro, P Mitocôndrias Cardiacas Piruvato |
title_short |
O Piruvato Melhora A Energética Mitocondrial Num Modelo Animal Ex-vivo de Isquemia Miocárdica Global |
title_full |
O Piruvato Melhora A Energética Mitocondrial Num Modelo Animal Ex-vivo de Isquemia Miocárdica Global |
title_fullStr |
O Piruvato Melhora A Energética Mitocondrial Num Modelo Animal Ex-vivo de Isquemia Miocárdica Global |
title_full_unstemmed |
O Piruvato Melhora A Energética Mitocondrial Num Modelo Animal Ex-vivo de Isquemia Miocárdica Global |
title_sort |
O Piruvato Melhora A Energética Mitocondrial Num Modelo Animal Ex-vivo de Isquemia Miocárdica Global |
author |
Monteiro, P |
author_facet |
Monteiro, P Duarte, AI Moreno, AJ Gonçalves, L Providência, LA |
author_role |
author |
author2 |
Duarte, AI Moreno, AJ Gonçalves, L Providência, LA |
author2_role |
author author author author |
dc.contributor.none.fl_str_mv |
RIHUC |
dc.contributor.author.fl_str_mv |
Monteiro, P Duarte, AI Moreno, AJ Gonçalves, L Providência, LA |
dc.subject.por.fl_str_mv |
Mitocôndrias Cardiacas Piruvato |
topic |
Mitocôndrias Cardiacas Piruvato |
description |
Pyruvate is an energy substrate with known cardioprotective activity. We know now that this is due not only to its antioxidant activity, but also to its reduction of intracellular acidosis, modulation of intracytosolic calcium and improvement of cardiomyocyte contractility. However, the role of cardiac mitochondria in such positive effects has only recently begun to be understood and the exact mechanisms of the effect of pyruvate on mitochondria are still largely unknown. Aiming to study the effect of pyruvate on cardiac mitochondrial function during acute ischemia, we used an ex-vivo animal model, perfused in a Langendorff system and then subjected to ischemia in the presence and absence of pyruvate. We evaluated the mitochondrial membrane electrical potential, the respiratory chain O2 consumption (and respiratory control ratio) and the energy charges generated with different energy substrates. We conclude that pyruvate has some effect on the mitochondrial oxidative system (by non-significantly improving the respiratory control ratio), but its main action is on the phosphorylation system, significantly decreasing the time taken to complete a phosphorylation cycle (lag phase) and improving ATP production (increase in energy charge), thus allowing better maintenance of mitochondrial membrane structure, with consequent improvement of the electrical potential after a phosphorylation cycle. These findings have enabled better understanding of the mechanisms behind pyruvate cytoprotection in ischemic cardiomyopathy, clearly highlighting the essential role of cardiac mitochondria in this process. |
publishDate |
2003 |
dc.date.none.fl_str_mv |
2003 2003-01-01T00:00:00Z 2008-12-12T15:17:55Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://hdl.handle.net/10400.4/341 |
url |
http://hdl.handle.net/10400.4/341 |
dc.language.iso.fl_str_mv |
por |
language |
por |
dc.relation.none.fl_str_mv |
Rev Port Cardiol. 2003 Jan;22(1):79-88 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
application/pdf |
dc.publisher.none.fl_str_mv |
Sociedade Portuguesa de Cardiologia |
publisher.none.fl_str_mv |
Sociedade Portuguesa de Cardiologia |
dc.source.none.fl_str_mv |
reponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação instacron:RCAAP |
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Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação |
instacron_str |
RCAAP |
institution |
RCAAP |
reponame_str |
Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
collection |
Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
repository.name.fl_str_mv |
Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação |
repository.mail.fl_str_mv |
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1799131696223748096 |