Transient Ca2+ depletion of the sarcoplasmic reticulum at the onset of reperfusion

Autores
Valverde, Carlos Alfredo; Kornyeyev, Dmytro; Ferreiro, Marcela; Petrosky, Azadé D.; Mattiazzi, Ramona Alicia; Escobar, Ariel Luis Manuel
Año de publicación
2010
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
AimsMyocardial stunning is a contractile dysfunction that occurs after a brief ischaemic insult. Substantial evidence supports that this dysfunction is triggered by Ca2+ overload during reperfusion. The aim of the present manuscript is to define the origin of this Ca2+ increase in the intact heart.Methods and resultsTo address this issue, Langendorff-perfused mouse hearts positioned on a pulsed local field fluorescence microscope and loaded with fluorescent dyes Rhod-2, Mag-fluo-4, and Di-8-ANEPPS, to assess cytosolic Ca2+, sarcoplasmic reticulum (SR) Ca2+, and transmembrane action potentials (AP), respectively, in the epicardial layer of the hearts, were submitted to 12 min of global ischaemia followed by reperfusion. Ischaemia increased cytosolic Ca2+ in association with a decrease in intracellular Ca2+ transients and a depression of Ca2+ transient kinetics, i.e. the rise time and decay time constant of Ca2+ transients were significantly prolonged. Reperfusion produced a transient increase in cytosolic Ca2+ (Ca2+ bump), which was temporally associated with a decrease in SR-Ca2+ content, as a mirror-like image. Caffeine pulses (20 mM) confirmed that SR-Ca2+ content was greatly diminished at the onset of reflow. The SR-Ca2+ decrease was associated with a decrease in Ca2+ transient amplitude and a shortening of AP duration mainly due to a decrease in phase 2.ConclusionTo the best of our knowledge, this is the first study in which SR-Ca2+ transients are recorded in the intact heart, revealing a previously unknown participation of SR on cytosolic Ca2+ overload upon reperfusion in the intact beating heart. Additionally, the associated shortening of phase 2 of the AP may provide a clue to explain early reperfusion arrhythmias.
Fil: Valverde, Carlos Alfredo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; Argentina
Fil: Kornyeyev, Dmytro. University of California; Estados Unidos
Fil: Ferreiro, Marcela. University of California; Estados Unidos
Fil: Petrosky, Azadé D.. University of California; Estados Unidos
Fil: Mattiazzi, Ramona Alicia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; Argentina
Fil: Escobar, Ariel Luis Manuel. University of California; Estados Unidos
Materia
Calcium
Fluorescence
Ischaemia/Reperfusion
Sarcoplasmic Reticulum
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:11336/61958
Acceder
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network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Transient Ca2+ depletion of the sarcoplasmic reticulum at the onset of reperfusionValverde, Carlos AlfredoKornyeyev, DmytroFerreiro, MarcelaPetrosky, Azadé D.Mattiazzi, Ramona AliciaEscobar, Ariel Luis ManuelCalciumFluorescenceIschaemia/ReperfusionSarcoplasmic Reticulumhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3AimsMyocardial stunning is a contractile dysfunction that occurs after a brief ischaemic insult. Substantial evidence supports that this dysfunction is triggered by Ca2+ overload during reperfusion. The aim of the present manuscript is to define the origin of this Ca2+ increase in the intact heart.Methods and resultsTo address this issue, Langendorff-perfused mouse hearts positioned on a pulsed local field fluorescence microscope and loaded with fluorescent dyes Rhod-2, Mag-fluo-4, and Di-8-ANEPPS, to assess cytosolic Ca2+, sarcoplasmic reticulum (SR) Ca2+, and transmembrane action potentials (AP), respectively, in the epicardial layer of the hearts, were submitted to 12 min of global ischaemia followed by reperfusion. Ischaemia increased cytosolic Ca2+ in association with a decrease in intracellular Ca2+ transients and a depression of Ca2+ transient kinetics, i.e. the rise time and decay time constant of Ca2+ transients were significantly prolonged. Reperfusion produced a transient increase in cytosolic Ca2+ (Ca2+ bump), which was temporally associated with a decrease in SR-Ca2+ content, as a mirror-like image. Caffeine pulses (20 mM) confirmed that SR-Ca2+ content was greatly diminished at the onset of reflow. The SR-Ca2+ decrease was associated with a decrease in Ca2+ transient amplitude and a shortening of AP duration mainly due to a decrease in phase 2.ConclusionTo the best of our knowledge, this is the first study in which SR-Ca2+ transients are recorded in the intact heart, revealing a previously unknown participation of SR on cytosolic Ca2+ overload upon reperfusion in the intact beating heart. Additionally, the associated shortening of phase 2 of the AP may provide a clue to explain early reperfusion arrhythmias.Fil: Valverde, Carlos Alfredo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; ArgentinaFil: Kornyeyev, Dmytro. University of California; Estados UnidosFil: Ferreiro, Marcela. University of California; Estados UnidosFil: Petrosky, Azadé D.. University of California; Estados UnidosFil: Mattiazzi, Ramona Alicia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; ArgentinaFil: Escobar, Ariel Luis Manuel. University of California; Estados UnidosOxford University Press2010-03info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/61958Valverde, Carlos Alfredo; Kornyeyev, Dmytro; Ferreiro, Marcela; Petrosky, Azadé D.; Mattiazzi, Ramona Alicia; et al.; Transient Ca2+ depletion of the sarcoplasmic reticulum at the onset of reperfusion; Oxford University Press; Cardiovascular Research; 85; 4; 3-2010; 671-6800008-6363CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1093/cvr/cvp371info:eu-repo/semantics/altIdentifier/url/https://academic.oup.com/cardiovascres/article/85/4/671/297526info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:44:39Zoai:ri.conicet.gov.ar:11336/61958instacron: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 09:44:39.993CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Transient Ca2+ depletion of the sarcoplasmic reticulum at the onset of reperfusion
title Transient Ca2+ depletion of the sarcoplasmic reticulum at the onset of reperfusion
spellingShingle Transient Ca2+ depletion of the sarcoplasmic reticulum at the onset of reperfusion
Valverde, Carlos Alfredo
Calcium
Fluorescence
Ischaemia/Reperfusion
Sarcoplasmic Reticulum
title_short Transient Ca2+ depletion of the sarcoplasmic reticulum at the onset of reperfusion
title_full Transient Ca2+ depletion of the sarcoplasmic reticulum at the onset of reperfusion
title_fullStr Transient Ca2+ depletion of the sarcoplasmic reticulum at the onset of reperfusion
title_full_unstemmed Transient Ca2+ depletion of the sarcoplasmic reticulum at the onset of reperfusion
title_sort Transient Ca2+ depletion of the sarcoplasmic reticulum at the onset of reperfusion
dc.creator.none.fl_str_mv Valverde, Carlos Alfredo
Kornyeyev, Dmytro
Ferreiro, Marcela
Petrosky, Azadé D.
Mattiazzi, Ramona Alicia
Escobar, Ariel Luis Manuel
author Valverde, Carlos Alfredo
author_facet Valverde, Carlos Alfredo
Kornyeyev, Dmytro
Ferreiro, Marcela
Petrosky, Azadé D.
Mattiazzi, Ramona Alicia
Escobar, Ariel Luis Manuel
author_role author
author2 Kornyeyev, Dmytro
Ferreiro, Marcela
Petrosky, Azadé D.
Mattiazzi, Ramona Alicia
Escobar, Ariel Luis Manuel
author2_role author
author
author
author
author
dc.subject.none.fl_str_mv Calcium
Fluorescence
Ischaemia/Reperfusion
Sarcoplasmic Reticulum
topic Calcium
Fluorescence
Ischaemia/Reperfusion
Sarcoplasmic Reticulum
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv AimsMyocardial stunning is a contractile dysfunction that occurs after a brief ischaemic insult. Substantial evidence supports that this dysfunction is triggered by Ca2+ overload during reperfusion. The aim of the present manuscript is to define the origin of this Ca2+ increase in the intact heart.Methods and resultsTo address this issue, Langendorff-perfused mouse hearts positioned on a pulsed local field fluorescence microscope and loaded with fluorescent dyes Rhod-2, Mag-fluo-4, and Di-8-ANEPPS, to assess cytosolic Ca2+, sarcoplasmic reticulum (SR) Ca2+, and transmembrane action potentials (AP), respectively, in the epicardial layer of the hearts, were submitted to 12 min of global ischaemia followed by reperfusion. Ischaemia increased cytosolic Ca2+ in association with a decrease in intracellular Ca2+ transients and a depression of Ca2+ transient kinetics, i.e. the rise time and decay time constant of Ca2+ transients were significantly prolonged. Reperfusion produced a transient increase in cytosolic Ca2+ (Ca2+ bump), which was temporally associated with a decrease in SR-Ca2+ content, as a mirror-like image. Caffeine pulses (20 mM) confirmed that SR-Ca2+ content was greatly diminished at the onset of reflow. The SR-Ca2+ decrease was associated with a decrease in Ca2+ transient amplitude and a shortening of AP duration mainly due to a decrease in phase 2.ConclusionTo the best of our knowledge, this is the first study in which SR-Ca2+ transients are recorded in the intact heart, revealing a previously unknown participation of SR on cytosolic Ca2+ overload upon reperfusion in the intact beating heart. Additionally, the associated shortening of phase 2 of the AP may provide a clue to explain early reperfusion arrhythmias.
Fil: Valverde, Carlos Alfredo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; Argentina
Fil: Kornyeyev, Dmytro. University of California; Estados Unidos
Fil: Ferreiro, Marcela. University of California; Estados Unidos
Fil: Petrosky, Azadé D.. University of California; Estados Unidos
Fil: Mattiazzi, Ramona Alicia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; Argentina
Fil: Escobar, Ariel Luis Manuel. University of California; Estados Unidos
description AimsMyocardial stunning is a contractile dysfunction that occurs after a brief ischaemic insult. Substantial evidence supports that this dysfunction is triggered by Ca2+ overload during reperfusion. The aim of the present manuscript is to define the origin of this Ca2+ increase in the intact heart.Methods and resultsTo address this issue, Langendorff-perfused mouse hearts positioned on a pulsed local field fluorescence microscope and loaded with fluorescent dyes Rhod-2, Mag-fluo-4, and Di-8-ANEPPS, to assess cytosolic Ca2+, sarcoplasmic reticulum (SR) Ca2+, and transmembrane action potentials (AP), respectively, in the epicardial layer of the hearts, were submitted to 12 min of global ischaemia followed by reperfusion. Ischaemia increased cytosolic Ca2+ in association with a decrease in intracellular Ca2+ transients and a depression of Ca2+ transient kinetics, i.e. the rise time and decay time constant of Ca2+ transients were significantly prolonged. Reperfusion produced a transient increase in cytosolic Ca2+ (Ca2+ bump), which was temporally associated with a decrease in SR-Ca2+ content, as a mirror-like image. Caffeine pulses (20 mM) confirmed that SR-Ca2+ content was greatly diminished at the onset of reflow. The SR-Ca2+ decrease was associated with a decrease in Ca2+ transient amplitude and a shortening of AP duration mainly due to a decrease in phase 2.ConclusionTo the best of our knowledge, this is the first study in which SR-Ca2+ transients are recorded in the intact heart, revealing a previously unknown participation of SR on cytosolic Ca2+ overload upon reperfusion in the intact beating heart. Additionally, the associated shortening of phase 2 of the AP may provide a clue to explain early reperfusion arrhythmias.
publishDate 2010
dc.date.none.fl_str_mv 2010-03
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/11336/61958
Valverde, Carlos Alfredo; Kornyeyev, Dmytro; Ferreiro, Marcela; Petrosky, Azadé D.; Mattiazzi, Ramona Alicia; et al.; Transient Ca2+ depletion of the sarcoplasmic reticulum at the onset of reperfusion; Oxford University Press; Cardiovascular Research; 85; 4; 3-2010; 671-680
0008-6363
CONICET Digital
CONICET
url http://hdl.handle.net/11336/61958
identifier_str_mv Valverde, Carlos Alfredo; Kornyeyev, Dmytro; Ferreiro, Marcela; Petrosky, Azadé D.; Mattiazzi, Ramona Alicia; et al.; Transient Ca2+ depletion of the sarcoplasmic reticulum at the onset of reperfusion; Oxford University Press; Cardiovascular Research; 85; 4; 3-2010; 671-680
0008-6363
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1093/cvr/cvp371
info:eu-repo/semantics/altIdentifier/url/https://academic.oup.com/cardiovascres/article/85/4/671/297526
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 Oxford University Press
publisher.none.fl_str_mv Oxford University Press
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 13.13397

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