Please use this identifier to cite or link to this item: https://hdl.handle.net/10316/107035
DC FieldValueLanguage
dc.contributor.authorMartins, Rui Miguel-
dc.contributor.authorTeodoro, João S.-
dc.contributor.authorFurtado, Emanuel-
dc.contributor.authorOliveira, Rui Caetano-
dc.contributor.authorTralhão, José Guilherme-
dc.contributor.authorRolo, Anabela Pinto-
dc.contributor.authorPalmeira, Carlos Marques-
dc.date.accessioned2023-05-10T10:12:35Z-
dc.date.available2023-05-10T10:12:35Z-
dc.date.issued2019-
dc.identifier.issn1449-1907pt
dc.identifier.urihttps://hdl.handle.net/10316/107035-
dc.description.abstractThe organ preservation paradigm has changed following the development of new ways to preserve organs. The use of machine perfusion to preserve organs appears to have several advantages compared with conventional static cold storage. For liver transplants, the temperature control provided by machine perfusion improves organ preservation. In this experimental study, we measured the effects of different temperatures on mitochondrial bioenergetics during the reperfusion phase. An experimental model of ex-vivo liver transplantation was developed in Wistar rats (Rattus norvegicus). After total hepatectomy, cold static preservation occurred at 4ºC and reperfusion was performed at 37ºC and 32ºC using a Langendorff system. We measured parameters associated with mitochondrial bioenergetics in the livers. Compared with the livers that underwent normothermic reperfusion, mild hypothermia during reperfusion caused significant increases in the mitochondrial membrane potential, the adenosine triphosphate content, and mitochondrial respiration, and a significant reduction in the lag phase (all P < 0.001). Mild hypothermia during reperfusion reduced the effect of ischemia-reperfusion injury on mitochondrial activity in liver tissue and promoted an increase in bioenergetic availability compared with normothermic reperfusion.pt
dc.language.isoengpt
dc.publisherIvyspring International Publisherpt
dc.relationSociedade Portuguesa de Transplantação (SPT)pt
dc.relationAstellas Pharmapt
dc.relationCentro de Investigação do Meio Ambiente, Genética e Oncobiologia (CIMAGO)pt
dc.relationGroupe IGL (Institut Georges Lopez)pt
dc.relationSFRH/BPD/94036/2013pt
dc.rightsopenAccesspt
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt
dc.subjecthypothermiapt
dc.subjectmitochondriapt
dc.subjectbioenergeticspt
dc.subjectadenosine triphosphatept
dc.subjectliver transplantationpt
dc.subject.meshAdenosine Triphosphatept
dc.subject.meshAnimalspt
dc.subject.meshDisease Models, Animalpt
dc.subject.meshHypothermia, Inducedpt
dc.subject.meshLiverpt
dc.subject.meshLiver Transplantationpt
dc.subject.meshMalept
dc.subject.meshMembrane Potential, Mitochondrialpt
dc.subject.meshMitochondria, Liverpt
dc.subject.meshOrgan Preservationpt
dc.subject.meshRats, Wistarpt
dc.subject.meshReperfusion Injurypt
dc.subject.meshTemperaturept
dc.titleMild hypothermia during the reperfusion phase protects mitochondrial bioenergetics against ischemia-reperfusion injury in an animal model of ex-vivo liver transplantation-an experimental studypt
dc.typearticle-
degois.publication.firstPage1304pt
degois.publication.lastPage1312pt
degois.publication.issue9pt
degois.publication.titleInternational Journal of Medical Sciencespt
dc.peerreviewedyespt
dc.identifier.doi10.7150/ijms.34617pt
degois.publication.volume16pt
dc.date.embargo2019-01-01*
uc.date.periodoEmbargo0pt
item.fulltextCom Texto completo-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.languageiso639-1en-
item.openairetypearticle-
item.cerifentitytypePublications-
item.grantfulltextopen-
crisitem.project.grantnoDETOXIFICATION OF FUEL OVERSUPPLY IN WAT THROUGH METABOLIC FUTILE CYCLING INDUCED BY BILE ACIDS-
crisitem.author.researchunitCNC - Center for Neuroscience and Cell Biology-
crisitem.author.researchunitCNC - Center for Neuroscience and Cell Biology-
crisitem.author.orcid0000-0002-1244-275X-
crisitem.author.orcid0000-0002-7202-8059-
crisitem.author.orcid0000-0003-3535-9630-
crisitem.author.orcid0000-0002-2639-7697-
Appears in Collections:FCTUC Ciências da Vida - Artigos em Revistas Internacionais
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