β₂-Adrenergic stimulation is involved in the contractile dysfunction of the stunned heart

Autores
Vittone, Leticia Beatriz; Said, María Matilde; Mattiazzi, Alicia Ramona
Año de publicación
2006
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Endogenous catecholamines released during myocardial ischemia have been considered both to aggravate cell injury and exacerbate arrhythmias and to exert a protective action on the post-ischemic contractile function. The present work was addressed to look for evidence to explain this controversy. The effects of cardiac catecholamine depletion and of α- and β-adrenoceptor (AR) blockade on the post-ischemic contractile dysfunction, as well as its possible relationship with cardiac oxidative stress, were studied in isolated and perfused rat hearts submitted to 20 min of ischemia and 30 min of reperfusion (stunning). Catecholamine depletion improves the contractile recovery in the stunned heart. This mechanical effect was associated with decreased levels of lipid peroxidation. A similar enhancement of the contractile function during reperfusion was detected after the simultaneous blockade of α₁- and β-ARs with prazosin plus propranolol. To ascertain which specific AR pathway was involved in the effects of catecholamines on the stunned heart, selective AR blockers, prazosin (α₁-blocker), atenolol (β₁-blocker), ICI 118,551 (β₂-blocker) and selective inhibitors of Gi-PI3K pathway (pertussis toxin and wortmannin) were alternatively combined. The results indicate that catecholamines released during ischemia exert a dual action on the contractile behavior of the stunned heart: a deleterious effect, related to the activation of the β₂-AR-Gi-PI3K-pathway, which was counteracted by a beneficial effect, triggered by the stimulation of α₁-AR. Neither the depression nor the enhancement of the post-ischemic contractile recovery were related with the increase in ROS formation induced by endogenous catecholamines.
Facultad de Ciencias Médicas
Centro de Investigaciones Cardiovasculares
Materia
Medicina
Stunned heart
Endogenous catecholamines
β2-adrenergic contractile effect
Nivel de accesibilidad
acceso abierto
Condiciones de uso
http://creativecommons.org/licenses/by-nc-sa/4.0/
Repositorio
SEDICI (UNLP)
Institución
Universidad Nacional de La Plata
OAI Identificador
oai:sedici.unlp.edu.ar:10915/130870

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oai_identifier_str oai:sedici.unlp.edu.ar:10915/130870
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network_name_str SEDICI (UNLP)
spelling β₂-Adrenergic stimulation is involved in the contractile dysfunction of the stunned heartVittone, Leticia BeatrizSaid, María MatildeMattiazzi, Alicia RamonaMedicinaStunned heartEndogenous catecholaminesβ2-adrenergic contractile effectEndogenous catecholamines released during myocardial ischemia have been considered both to aggravate cell injury and exacerbate arrhythmias and to exert a protective action on the post-ischemic contractile function. The present work was addressed to look for evidence to explain this controversy. The effects of cardiac catecholamine depletion and of α- and β-adrenoceptor (AR) blockade on the post-ischemic contractile dysfunction, as well as its possible relationship with cardiac oxidative stress, were studied in isolated and perfused rat hearts submitted to 20 min of ischemia and 30 min of reperfusion (stunning). Catecholamine depletion improves the contractile recovery in the stunned heart. This mechanical effect was associated with decreased levels of lipid peroxidation. A similar enhancement of the contractile function during reperfusion was detected after the simultaneous blockade of α₁- and β-ARs with prazosin plus propranolol. To ascertain which specific AR pathway was involved in the effects of catecholamines on the stunned heart, selective AR blockers, prazosin (α₁-blocker), atenolol (β₁-blocker), ICI 118,551 (β₂-blocker) and selective inhibitors of G<sub>i</sub>-PI3K pathway (pertussis toxin and wortmannin) were alternatively combined. The results indicate that catecholamines released during ischemia exert a dual action on the contractile behavior of the stunned heart: a deleterious effect, related to the activation of the β₂-AR-G<sub>i</sub>-PI3K-pathway, which was counteracted by a beneficial effect, triggered by the stimulation of α₁-AR. Neither the depression nor the enhancement of the post-ischemic contractile recovery were related with the increase in ROS formation induced by endogenous catecholamines.Facultad de Ciencias MédicasCentro de Investigaciones Cardiovasculares2006-04info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionArticulohttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdf60-70http://sedici.unlp.edu.ar/handle/10915/130870enginfo:eu-repo/semantics/altIdentifier/issn/0028-1298info:eu-repo/semantics/altIdentifier/issn/1432-1912info:eu-repo/semantics/altIdentifier/doi/10.1007/s00210-006-0045-6info:eu-repo/semantics/altIdentifier/pmid/16575588info:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by-nc-sa/4.0/Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)reponame:SEDICI (UNLP)instname:Universidad Nacional de La Platainstacron:UNLP2025-09-03T11:04:43Zoai:sedici.unlp.edu.ar:10915/130870Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292025-09-03 11:04:44.195SEDICI (UNLP) - Universidad Nacional de La Platafalse
dc.title.none.fl_str_mv β₂-Adrenergic stimulation is involved in the contractile dysfunction of the stunned heart
title β₂-Adrenergic stimulation is involved in the contractile dysfunction of the stunned heart
spellingShingle β₂-Adrenergic stimulation is involved in the contractile dysfunction of the stunned heart
Vittone, Leticia Beatriz
Medicina
Stunned heart
Endogenous catecholamines
β2-adrenergic contractile effect
title_short β₂-Adrenergic stimulation is involved in the contractile dysfunction of the stunned heart
title_full β₂-Adrenergic stimulation is involved in the contractile dysfunction of the stunned heart
title_fullStr β₂-Adrenergic stimulation is involved in the contractile dysfunction of the stunned heart
title_full_unstemmed β₂-Adrenergic stimulation is involved in the contractile dysfunction of the stunned heart
title_sort β₂-Adrenergic stimulation is involved in the contractile dysfunction of the stunned heart
dc.creator.none.fl_str_mv Vittone, Leticia Beatriz
Said, María Matilde
Mattiazzi, Alicia Ramona
author Vittone, Leticia Beatriz
author_facet Vittone, Leticia Beatriz
Said, María Matilde
Mattiazzi, Alicia Ramona
author_role author
author2 Said, María Matilde
Mattiazzi, Alicia Ramona
author2_role author
author
dc.subject.none.fl_str_mv Medicina
Stunned heart
Endogenous catecholamines
β2-adrenergic contractile effect
topic Medicina
Stunned heart
Endogenous catecholamines
β2-adrenergic contractile effect
dc.description.none.fl_txt_mv Endogenous catecholamines released during myocardial ischemia have been considered both to aggravate cell injury and exacerbate arrhythmias and to exert a protective action on the post-ischemic contractile function. The present work was addressed to look for evidence to explain this controversy. The effects of cardiac catecholamine depletion and of α- and β-adrenoceptor (AR) blockade on the post-ischemic contractile dysfunction, as well as its possible relationship with cardiac oxidative stress, were studied in isolated and perfused rat hearts submitted to 20 min of ischemia and 30 min of reperfusion (stunning). Catecholamine depletion improves the contractile recovery in the stunned heart. This mechanical effect was associated with decreased levels of lipid peroxidation. A similar enhancement of the contractile function during reperfusion was detected after the simultaneous blockade of α₁- and β-ARs with prazosin plus propranolol. To ascertain which specific AR pathway was involved in the effects of catecholamines on the stunned heart, selective AR blockers, prazosin (α₁-blocker), atenolol (β₁-blocker), ICI 118,551 (β₂-blocker) and selective inhibitors of G<sub>i</sub>-PI3K pathway (pertussis toxin and wortmannin) were alternatively combined. The results indicate that catecholamines released during ischemia exert a dual action on the contractile behavior of the stunned heart: a deleterious effect, related to the activation of the β₂-AR-G<sub>i</sub>-PI3K-pathway, which was counteracted by a beneficial effect, triggered by the stimulation of α₁-AR. Neither the depression nor the enhancement of the post-ischemic contractile recovery were related with the increase in ROS formation induced by endogenous catecholamines.
Facultad de Ciencias Médicas
Centro de Investigaciones Cardiovasculares
description Endogenous catecholamines released during myocardial ischemia have been considered both to aggravate cell injury and exacerbate arrhythmias and to exert a protective action on the post-ischemic contractile function. The present work was addressed to look for evidence to explain this controversy. The effects of cardiac catecholamine depletion and of α- and β-adrenoceptor (AR) blockade on the post-ischemic contractile dysfunction, as well as its possible relationship with cardiac oxidative stress, were studied in isolated and perfused rat hearts submitted to 20 min of ischemia and 30 min of reperfusion (stunning). Catecholamine depletion improves the contractile recovery in the stunned heart. This mechanical effect was associated with decreased levels of lipid peroxidation. A similar enhancement of the contractile function during reperfusion was detected after the simultaneous blockade of α₁- and β-ARs with prazosin plus propranolol. To ascertain which specific AR pathway was involved in the effects of catecholamines on the stunned heart, selective AR blockers, prazosin (α₁-blocker), atenolol (β₁-blocker), ICI 118,551 (β₂-blocker) and selective inhibitors of G<sub>i</sub>-PI3K pathway (pertussis toxin and wortmannin) were alternatively combined. The results indicate that catecholamines released during ischemia exert a dual action on the contractile behavior of the stunned heart: a deleterious effect, related to the activation of the β₂-AR-G<sub>i</sub>-PI3K-pathway, which was counteracted by a beneficial effect, triggered by the stimulation of α₁-AR. Neither the depression nor the enhancement of the post-ischemic contractile recovery were related with the increase in ROS formation induced by endogenous catecholamines.
publishDate 2006
dc.date.none.fl_str_mv 2006-04
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
Articulo
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://sedici.unlp.edu.ar/handle/10915/130870
url http://sedici.unlp.edu.ar/handle/10915/130870
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/issn/0028-1298
info:eu-repo/semantics/altIdentifier/issn/1432-1912
info:eu-repo/semantics/altIdentifier/doi/10.1007/s00210-006-0045-6
info:eu-repo/semantics/altIdentifier/pmid/16575588
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
http://creativecommons.org/licenses/by-nc-sa/4.0/
Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)
eu_rights_str_mv openAccess
rights_invalid_str_mv http://creativecommons.org/licenses/by-nc-sa/4.0/
Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)
dc.format.none.fl_str_mv application/pdf
60-70
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instname:Universidad Nacional de La Plata
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reponame_str SEDICI (UNLP)
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instname_str Universidad Nacional de La Plata
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repository.name.fl_str_mv SEDICI (UNLP) - Universidad Nacional de La Plata
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