Cobalt chloride protects the heart after a global ischemic insult

Autores
Gutierrez, Christopher; Farcy, Nicole; Bonazzola, Patricia; Castilla, Rocio Soledad
Año de publicación
2020
Idioma
inglés
Tipo de recurso
documento de conferencia
Estado
versión publicada
Descripción
Introduction: Ischemia-reperfusion (I/R) is one of the main cardiovascular risk factors and leads to heart contractile and energy dysfunction. I/R-induced damage is reduced by ischemic postconditioning. CoCl₂ has properties to function as a postconditioning agent, since it can trigger transcriptional changes that resemble the response to a hypoxic event under normoxic conditions.Objectives: To evaluate CoCl₂ as a postconditioning therapeutic tool after a myocardial and arterial I/R.Materials and Methods: Isolated adult Wistar rats hearts were arterially perfused at 37ºC by Langendorff method, paced at 3 Hz, exposed to 30 min ischemia followed by 45 min reperfusion (R) in the presence or absence of 0.23 mM CoCl2 which was maintained or removed after 20 min of R.Aortic contractility was evaluated in an isolated organ bath trough incubation with cumulative noradrenaline (NA) doses. After NA washing, 20 min of simulated arterial ischemia (SI) and R with or without CoCl₂ was performed, and NA response was re-evaluated.Results: During R, the presence of CoCl₂ did not alter the cardiac resting pressure, nor the perfusion pressure, but increased the developed pressure (p<0.05) until 20 min which then descend reaching controls values. This decrease was prevented when CoCl₂ was eliminated at 20 min of R. CoCl₂ in R increased the contractile economy (P/Ht) and decreased the cardiac damaged area (p<0.05) and the incidence of arrhythmias (p<0.001).Post-SI arterial contractility increased at the lowest NA dose but not at higher ones. CoCl₂ in post ?SI R did not affect arterial force, but decreased NA sensitivity (EC 50: control: 10-7.5, CoCl2: 10-6.5 M) and the maximum contractile response.Conclusion: The use of CoCl₂ after an ischemic event attenuates the cardiac damage produced at least during the first 25 min of R and reduces the arterial adrenergic contractile response. These results support the use of CoCl₂ as a potential cardioprotective tool of clinical relevance.
Fil: Gutierrez, Christopher. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Oficina de Coordinacion Administrativa Houssay. Instituto Alberto C. Taquini de Investigaciones En Medicina Traslacional. - Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiologicas "prof. Dr. Alberto C. Taquini". Instituto Alberto C. Taquini de Investigaciones En Medicina Traslacional.; Argentina
Fil: Farcy, Nicole. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Oficina de Coordinacion Administrativa Houssay. Instituto Alberto C. Taquini de Investigaciones En Medicina Traslacional. - Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiologicas "prof. Dr. Alberto C. Taquini". Instituto Alberto C. Taquini de Investigaciones En Medicina Traslacional.; Argentina
Fil: Bonazzola, Patricia. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Oficina de Coordinacion Administrativa Houssay. Instituto Alberto C. Taquini de Investigaciones En Medicina Traslacional. - Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiologicas "prof. Dr. Alberto C. Taquini". Instituto Alberto C. Taquini de Investigaciones En Medicina Traslacional.; Argentina
Fil: Castilla, Rocio Soledad. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Oficina de Coordinacion Administrativa Houssay. Instituto Alberto C. Taquini de Investigaciones En Medicina Traslacional. - Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiologicas "prof. Dr. Alberto C. Taquini". Instituto Alberto C. Taquini de Investigaciones En Medicina Traslacional.; Argentina
LXV Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXVIII Reunión Anual de la Sociedad Argentina de Inmunología y Reunión Anual de la Sociedad Argentina de Fisiología
Argentina
Sociedad Argentina de Investigación Clínica
Sociedad Argentina de Inmunología
Sociedad Argentina de Fisiología
Materia
POSTCONDICIONAMIENTO
CLORURO DE COBALTO
CARDIOPROTECCION
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/198974

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oai_identifier_str oai:ri.conicet.gov.ar:11336/198974
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Cobalt chloride protects the heart after a global ischemic insultGutierrez, ChristopherFarcy, NicoleBonazzola, PatriciaCastilla, Rocio SoledadPOSTCONDICIONAMIENTOCLORURO DE COBALTOCARDIOPROTECCIONhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Introduction: Ischemia-reperfusion (I/R) is one of the main cardiovascular risk factors and leads to heart contractile and energy dysfunction. I/R-induced damage is reduced by ischemic postconditioning. CoCl₂ has properties to function as a postconditioning agent, since it can trigger transcriptional changes that resemble the response to a hypoxic event under normoxic conditions.Objectives: To evaluate CoCl₂ as a postconditioning therapeutic tool after a myocardial and arterial I/R.Materials and Methods: Isolated adult Wistar rats hearts were arterially perfused at 37ºC by Langendorff method, paced at 3 Hz, exposed to 30 min ischemia followed by 45 min reperfusion (R) in the presence or absence of 0.23 mM CoCl2 which was maintained or removed after 20 min of R.Aortic contractility was evaluated in an isolated organ bath trough incubation with cumulative noradrenaline (NA) doses. After NA washing, 20 min of simulated arterial ischemia (SI) and R with or without CoCl₂ was performed, and NA response was re-evaluated.Results: During R, the presence of CoCl₂ did not alter the cardiac resting pressure, nor the perfusion pressure, but increased the developed pressure (p<0.05) until 20 min which then descend reaching controls values. This decrease was prevented when CoCl₂ was eliminated at 20 min of R. CoCl₂ in R increased the contractile economy (P/Ht) and decreased the cardiac damaged area (p<0.05) and the incidence of arrhythmias (p<0.001).Post-SI arterial contractility increased at the lowest NA dose but not at higher ones. CoCl₂ in post ?SI R did not affect arterial force, but decreased NA sensitivity (EC 50: control: 10-7.5, CoCl2: 10-6.5 M) and the maximum contractile response.Conclusion: The use of CoCl₂ after an ischemic event attenuates the cardiac damage produced at least during the first 25 min of R and reduces the arterial adrenergic contractile response. These results support the use of CoCl₂ as a potential cardioprotective tool of clinical relevance.Fil: Gutierrez, Christopher. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Oficina de Coordinacion Administrativa Houssay. Instituto Alberto C. Taquini de Investigaciones En Medicina Traslacional. - Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiologicas "prof. Dr. Alberto C. Taquini". Instituto Alberto C. Taquini de Investigaciones En Medicina Traslacional.; ArgentinaFil: Farcy, Nicole. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Oficina de Coordinacion Administrativa Houssay. Instituto Alberto C. Taquini de Investigaciones En Medicina Traslacional. - Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiologicas "prof. Dr. Alberto C. Taquini". Instituto Alberto C. Taquini de Investigaciones En Medicina Traslacional.; ArgentinaFil: Bonazzola, Patricia. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Oficina de Coordinacion Administrativa Houssay. Instituto Alberto C. Taquini de Investigaciones En Medicina Traslacional. - Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiologicas "prof. Dr. Alberto C. Taquini". Instituto Alberto C. Taquini de Investigaciones En Medicina Traslacional.; ArgentinaFil: Castilla, Rocio Soledad. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Oficina de Coordinacion Administrativa Houssay. Instituto Alberto C. Taquini de Investigaciones En Medicina Traslacional. - Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiologicas "prof. Dr. Alberto C. Taquini". Instituto Alberto C. Taquini de Investigaciones En Medicina Traslacional.; ArgentinaLXV Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXVIII Reunión Anual de la Sociedad Argentina de Inmunología y Reunión Anual de la Sociedad Argentina de FisiologíaArgentinaSociedad Argentina de Investigación ClínicaSociedad Argentina de InmunologíaSociedad Argentina de FisiologíaFundación Revista Medicina2020info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/conferenceObjectReuniónJournalhttp://purl.org/coar/resource_type/c_5794info:ar-repo/semantics/documentoDeConferenciaapplication/pdfapplication/mswordapplication/pdfhttp://hdl.handle.net/11336/198974Cobalt chloride protects the heart after a global ischemic insult; LXV Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXVIII Reunión Anual de la Sociedad Argentina de Inmunología y Reunión Anual de la Sociedad Argentina de Fisiología; Argentina; 2020; 54-54CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.saic.org.ar/reunion-anualNacionalinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:44:34Zoai:ri.conicet.gov.ar:11336/198974instacron: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:34982025-09-29 10:44:34.285CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Cobalt chloride protects the heart after a global ischemic insult
title Cobalt chloride protects the heart after a global ischemic insult
spellingShingle Cobalt chloride protects the heart after a global ischemic insult
Gutierrez, Christopher
POSTCONDICIONAMIENTO
CLORURO DE COBALTO
CARDIOPROTECCION
title_short Cobalt chloride protects the heart after a global ischemic insult
title_full Cobalt chloride protects the heart after a global ischemic insult
title_fullStr Cobalt chloride protects the heart after a global ischemic insult
title_full_unstemmed Cobalt chloride protects the heart after a global ischemic insult
title_sort Cobalt chloride protects the heart after a global ischemic insult
dc.creator.none.fl_str_mv Gutierrez, Christopher
Farcy, Nicole
Bonazzola, Patricia
Castilla, Rocio Soledad
author Gutierrez, Christopher
author_facet Gutierrez, Christopher
Farcy, Nicole
Bonazzola, Patricia
Castilla, Rocio Soledad
author_role author
author2 Farcy, Nicole
Bonazzola, Patricia
Castilla, Rocio Soledad
author2_role author
author
author
dc.subject.none.fl_str_mv POSTCONDICIONAMIENTO
CLORURO DE COBALTO
CARDIOPROTECCION
topic POSTCONDICIONAMIENTO
CLORURO DE COBALTO
CARDIOPROTECCION
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Introduction: Ischemia-reperfusion (I/R) is one of the main cardiovascular risk factors and leads to heart contractile and energy dysfunction. I/R-induced damage is reduced by ischemic postconditioning. CoCl₂ has properties to function as a postconditioning agent, since it can trigger transcriptional changes that resemble the response to a hypoxic event under normoxic conditions.Objectives: To evaluate CoCl₂ as a postconditioning therapeutic tool after a myocardial and arterial I/R.Materials and Methods: Isolated adult Wistar rats hearts were arterially perfused at 37ºC by Langendorff method, paced at 3 Hz, exposed to 30 min ischemia followed by 45 min reperfusion (R) in the presence or absence of 0.23 mM CoCl2 which was maintained or removed after 20 min of R.Aortic contractility was evaluated in an isolated organ bath trough incubation with cumulative noradrenaline (NA) doses. After NA washing, 20 min of simulated arterial ischemia (SI) and R with or without CoCl₂ was performed, and NA response was re-evaluated.Results: During R, the presence of CoCl₂ did not alter the cardiac resting pressure, nor the perfusion pressure, but increased the developed pressure (p<0.05) until 20 min which then descend reaching controls values. This decrease was prevented when CoCl₂ was eliminated at 20 min of R. CoCl₂ in R increased the contractile economy (P/Ht) and decreased the cardiac damaged area (p<0.05) and the incidence of arrhythmias (p<0.001).Post-SI arterial contractility increased at the lowest NA dose but not at higher ones. CoCl₂ in post ?SI R did not affect arterial force, but decreased NA sensitivity (EC 50: control: 10-7.5, CoCl2: 10-6.5 M) and the maximum contractile response.Conclusion: The use of CoCl₂ after an ischemic event attenuates the cardiac damage produced at least during the first 25 min of R and reduces the arterial adrenergic contractile response. These results support the use of CoCl₂ as a potential cardioprotective tool of clinical relevance.
Fil: Gutierrez, Christopher. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Oficina de Coordinacion Administrativa Houssay. Instituto Alberto C. Taquini de Investigaciones En Medicina Traslacional. - Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiologicas "prof. Dr. Alberto C. Taquini". Instituto Alberto C. Taquini de Investigaciones En Medicina Traslacional.; Argentina
Fil: Farcy, Nicole. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Oficina de Coordinacion Administrativa Houssay. Instituto Alberto C. Taquini de Investigaciones En Medicina Traslacional. - Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiologicas "prof. Dr. Alberto C. Taquini". Instituto Alberto C. Taquini de Investigaciones En Medicina Traslacional.; Argentina
Fil: Bonazzola, Patricia. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Oficina de Coordinacion Administrativa Houssay. Instituto Alberto C. Taquini de Investigaciones En Medicina Traslacional. - Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiologicas "prof. Dr. Alberto C. Taquini". Instituto Alberto C. Taquini de Investigaciones En Medicina Traslacional.; Argentina
Fil: Castilla, Rocio Soledad. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Oficina de Coordinacion Administrativa Houssay. Instituto Alberto C. Taquini de Investigaciones En Medicina Traslacional. - Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiologicas "prof. Dr. Alberto C. Taquini". Instituto Alberto C. Taquini de Investigaciones En Medicina Traslacional.; Argentina
LXV Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXVIII Reunión Anual de la Sociedad Argentina de Inmunología y Reunión Anual de la Sociedad Argentina de Fisiología
Argentina
Sociedad Argentina de Investigación Clínica
Sociedad Argentina de Inmunología
Sociedad Argentina de Fisiología
description Introduction: Ischemia-reperfusion (I/R) is one of the main cardiovascular risk factors and leads to heart contractile and energy dysfunction. I/R-induced damage is reduced by ischemic postconditioning. CoCl₂ has properties to function as a postconditioning agent, since it can trigger transcriptional changes that resemble the response to a hypoxic event under normoxic conditions.Objectives: To evaluate CoCl₂ as a postconditioning therapeutic tool after a myocardial and arterial I/R.Materials and Methods: Isolated adult Wistar rats hearts were arterially perfused at 37ºC by Langendorff method, paced at 3 Hz, exposed to 30 min ischemia followed by 45 min reperfusion (R) in the presence or absence of 0.23 mM CoCl2 which was maintained or removed after 20 min of R.Aortic contractility was evaluated in an isolated organ bath trough incubation with cumulative noradrenaline (NA) doses. After NA washing, 20 min of simulated arterial ischemia (SI) and R with or without CoCl₂ was performed, and NA response was re-evaluated.Results: During R, the presence of CoCl₂ did not alter the cardiac resting pressure, nor the perfusion pressure, but increased the developed pressure (p<0.05) until 20 min which then descend reaching controls values. This decrease was prevented when CoCl₂ was eliminated at 20 min of R. CoCl₂ in R increased the contractile economy (P/Ht) and decreased the cardiac damaged area (p<0.05) and the incidence of arrhythmias (p<0.001).Post-SI arterial contractility increased at the lowest NA dose but not at higher ones. CoCl₂ in post ?SI R did not affect arterial force, but decreased NA sensitivity (EC 50: control: 10-7.5, CoCl2: 10-6.5 M) and the maximum contractile response.Conclusion: The use of CoCl₂ after an ischemic event attenuates the cardiac damage produced at least during the first 25 min of R and reduces the arterial adrenergic contractile response. These results support the use of CoCl₂ as a potential cardioprotective tool of clinical relevance.
publishDate 2020
dc.date.none.fl_str_mv 2020
dc.type.none.fl_str_mv info:eu-repo/semantics/publishedVersion
info:eu-repo/semantics/conferenceObject
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info:ar-repo/semantics/documentoDeConferencia
status_str publishedVersion
format conferenceObject
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/198974
Cobalt chloride protects the heart after a global ischemic insult; LXV Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXVIII Reunión Anual de la Sociedad Argentina de Inmunología y Reunión Anual de la Sociedad Argentina de Fisiología; Argentina; 2020; 54-54
CONICET Digital
CONICET
url http://hdl.handle.net/11336/198974
identifier_str_mv Cobalt chloride protects the heart after a global ischemic insult; LXV Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXVIII Reunión Anual de la Sociedad Argentina de Inmunología y Reunión Anual de la Sociedad Argentina de Fisiología; Argentina; 2020; 54-54
CONICET Digital
CONICET
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language eng
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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/
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application/msword
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dc.publisher.none.fl_str_mv Fundación Revista Medicina
publisher.none.fl_str_mv Fundación Revista Medicina
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