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dc.contributor.author
Donato, Martín
dc.contributor.author
Goyeneche, María A.
dc.contributor.author
Garces, Mariana
dc.contributor.author
Marchini, Timoteo Oscar
dc.contributor.author
Pérez, Virginia
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del Mauro, Julieta
dc.contributor.author
Höcht, Christian
dc.contributor.author
Rodríguez, Manuel
dc.contributor.author
Evelson, Pablo Andrés
dc.contributor.author
Gelpi, Ricardo Jorge
dc.date.available
2020-01-15T18:16:13Z
dc.date.issued
2016-06
dc.identifier.citation
Donato, Martín; Goyeneche, María A.; Garces, Mariana; Marchini, Timoteo Oscar; Pérez, Virginia; et al.; Myocardial triggers involved in activation of remote ischaemic preconditioning; Wiley Blackwell Publishing, Inc; Experimental Physiology; 101; 6; 6-2016; 708-716
dc.identifier.issn
0958-0670
dc.identifier.uri
http://hdl.handle.net/11336/94769
dc.description.abstract
New Findings What is the central question of this study? Ischaemia–reperfusion of peripheral tissues protects the heart from subsequent myocardial ischaemia–reperfusion injury, a phenomenon referred to as remote ischaemic preconditioning (rIPC). This study evaluated the possible myocardial triggers of rIPC. What is the main finding and its importance? Remote ischaemic preconditioning reduces infarct size through a vagal pathway and a mechanism involving phosphorylation of Akt and endothelial nitric oxide synthase, opening of mitochondrial ATP‐dependent K+ channels and an increase in mitochondrial H2O2 production. All these phenomena occur before the myocardial ischaemia; hence, they could act as ‘triggers’ of rIPC. It has been proposed that remote ischaemic preconditioning (rIPC) activates a parasympathetic neural pathway. However, the myocardial intracellular mechanism of rIPC remains unclear. Here, we characterized some of the intracellular signals participating as rIPC triggers. Isolated rat hearts were subjected to 30 min of global ischaemia and 120 min of reperfusion (Non‐rIPC group). In a second group, before the isolation of the heart, an rIPC protocol (three cycles of hindlimb ischaemia–reperfusion) was performed. The infarct size was measured with tetrazolium staining. Expression/phosphorylation of Akt and endothelial nitric oxide synthase (eNOS) and mitochondrial H2O2 production were evaluated at the end of the rIPC protocol, before myocardial ischaemia–reperfusion. The rIPC significantly decreased the infarct size and induced Akt and eNOS phosphorylation. The protective effect on infarct size was abolished by cervical vagal section, l‐NAME (an NO synthesis inhibitor) and 5‐hydroxydecanoate (a mitochondrial ATP‐dependent K+ channel blocker). Mitochondrial production of H2O2 was increased by rIPC, whereas it was abolished by cervical vagal section, l‐NAME and 5‐hydroxydecanoate. We conclude that rIPC activates a parasympathetic vagal pathway and a mechanism involving the phosphorylation of Akt and eNOS, the opening of mitochondrial ATP‐dependent K+ channels and the release of H2O2 by the mitochondria. All these phenomena occur before myocardial ischaemia and could act as triggers of rIPC.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Wiley Blackwell Publishing, Inc
dc.rights
info:eu-repo/semantics/restrictedAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
myocardial infarction
dc.subject
remote preconditioning
dc.subject
cardioprotection
dc.subject.classification
Otras Ciencias de la Salud
dc.subject.classification
Ciencias de la Salud
dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD
dc.title
Myocardial triggers involved in activation of remote ischaemic preconditioning
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2019-12-27T13:58:56Z
dc.journal.volume
101
dc.journal.number
6
dc.journal.pagination
708-716
dc.journal.pais
Reino Unido
dc.journal.ciudad
Londres
dc.journal.title
Experimental Physiology
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://physoc.onlinelibrary.wiley.com/doi/full/10.1113/EP085535
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1113/EP085535


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