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
- Institución
- Universidad Nacional de La Plata
- OAI Identificador
- oai:sedici.unlp.edu.ar:10915/130870
Ver los metadatos del registro completo
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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 |
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http://sedici.unlp.edu.ar/handle/10915/130870 |
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eng |
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