Modelo experimental de perfusão pulmonar ex vivo em ratos: avaliação histopatológica e de apoptose celular em pulmões preservados com solução de baixo potássio dextrana vs. solução histidina-triptofano-cetoglutarato

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dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.authorSIMOES, Edson Azevedo
dc.contributor.authorCARDOSO, Paulo Francisco Guerreiro
dc.contributor.authorPEGO-FERNANDES, Paulo Manuel
dc.contributor.authorCANZIAN, Mauro
dc.contributor.authorPAZETTI, Rogerio
dc.contributor.authorBRAGA, Karina Andriguetti de Oliveira
dc.contributor.authorNEPOMUCENO, Natalia Aparecida
dc.contributor.authorJATENE, Fabio Biscegli
dc.date.accessioned2013-07-30T14:34:59Z
dc.date.available2013-07-30T14:34:59Z
dc.date.issued2012
dc.description.abstractObjective: To compare histopathological findings and the degree of apoptosis among rat lungs preserved with low-potassium dextran (LPD) solution, histidine-tryptophan-ketoglutarate (HTK) solution, or normal saline (NS) at two ischemia periods (6 h and 12 h) using an experimental rat model of ex vivo lung perfusion. Methods: Sixty Wistar rats were anesthetized, randomized, and submitted to antegrade perfusion via pulmonary artery with one of the preservation solutions. Following en bloc extraction, the heart-lung blocks were preserved for 6 h or 12 h at 4 degrees C and then reperfused with homologous blood for 60 min in an ex vivo lung perfusion system. At the end of the reperfusion, fragments of the middle lobe were extracted and processed for histopathological examination. The parameters evaluated were congestion, alveolar edema, alveolar hemorrhage, inflammatory infiltrate, and interstitial infiltrate. The degree of apoptosis was assessed using the TdT-mediated dUTP nick end labeling method. Results: The histopathological examination showed that all of the lungs preserved with NS presented alveolar edema after 12 h of ischemia. There were no statistically significant differences among the groups in terms of the degree of apoptosis. Conclusions: In this study, the histopathological and apoptosis findings were similar with the use of either LPD or HTK solutions, whereas the occurrence of edema was significantly more common with the use of NS.
dc.description.abstractObjetivo: Comparar os achados histopatológicos e de apoptose em pulmões de ratos preservados em soluções low-potassium dextran (LPD, baixo potássio dextrana), histidine-tryptophan-ketoglutarate (HTK, histidina-triptofano-cetoglutarato) ou salina normal (SN) em 6 h e 12 h de isquemia pela utilização de um modelo experimental de perfusão pulmonar ex vivo. Métodos: Sessenta ratos Wistar foram anestesiados, randomizados e submetidos à perfusão anterógrada pela artéria pulmonar com uma das soluções preservadoras. Após a extração, os blocos cardiopulmonares foram preservados por 6 ou 12 h a 4°C, sendo então reperfundidos com sangue homólogo em um sistema de perfusão ex vivo durante 60 min. Ao final da reperfusão, fragmentos do lobo médio foram extraídos e processados para histopatologia, sendo avaliados os seguintes parâmetros: congestão, edema alveolar, hemorragia alveolar, hemorragia, infiltrado inflamatório e infiltrado intersticial. O grau de apoptose foi avaliado pelo método TdT-mediated dUTP nick end labeling. Resultados: A histopatologia demonstrou que todos os pulmões preservados com SN apresentaram edema alveolar após 12 h de isquemia. Não houve diferenças em relação ao grau de apoptose nos grupos estudados. Conclusões: No presente estudo, os achados histopatológicos e de apoptose foram semelhantes com o uso das soluções LPD e HTK, enquanto a presença de edema foi significativamente maior com o uso de SN.
dc.description.indexMEDLINE
dc.identifier.citationJORNAL BRASILEIRO DE PNEUMOLOGIA, v.38, n.4, p.461-469, 2012
dc.identifier.doi10.1590/s1806-37132012000400008
dc.identifier.issn1806-3713
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/230
dc.language.isopor
dc.language.isoeng
dc.publisherSOC BRASILEIRA PNEUMOLOGIA TISIOLOGIA
dc.relation.ispartofJornal Brasileiro de Pneumologia
dc.rightsopenAccess
dc.rights.holderCopyright SOC BRASILEIRA PNEUMOLOGIA TISIOLOGIA
dc.subjectOrgan preservation
dc.subjectOrgan preservation solutions
dc.subjectLung transplantation
dc.subjectReperfusion injury
dc.subjectApoptosis
dc.subjectPreservação de órgãos
dc.subjectSoluções para preservação de órgãos
dc.subjectTransplante de pulmão
dc.subjectTraumatismo por reperfusão
dc.subjectApoptose
dc.subject.otherischemia-reperfusion injury
dc.subject.otherbronchiolitis obliterans syndrome
dc.subject.othertransplantation increases risk
dc.subject.othereuro-collins solution
dc.subject.otherliver-transplantation
dc.subject.otherpreservation
dc.subject.otherprostacyclin
dc.subject.othersuperior
dc.subject.otherperfadex
dc.subject.otherhtk
dc.subject.wosRespiratory System
dc.titleModelo experimental de perfusão pulmonar ex vivo em ratos: avaliação histopatológica e de apoptose celular em pulmões preservados com solução de baixo potássio dextrana vs. solução histidina-triptofano-cetoglutarato
dc.title.alternativeAn experimental rat model of ex vivo lung perfusion for the assessment of lungs regarding histopathological findings and apoptosis: low-potassium dextran vs. histidine-tryptophan-ketoglutarate
dc.typearticle
dc.type.categoryoriginal article
dc.type.versionpublishedVersion
dspace.entity.typePublication
hcfmusp.citation.scopus4
hcfmusp.contributor.author-fmusphcEDSON AZEVEDO SIMOES
hcfmusp.contributor.author-fmusphcPAULO FRANCISCO GUERREIRO CARDOSO
hcfmusp.contributor.author-fmusphcPAULO MANUEL PEGO FERNANDES
hcfmusp.contributor.author-fmusphcMAURO CANZIAN
hcfmusp.contributor.author-fmusphcROGERIO PAZETTI
hcfmusp.contributor.author-fmusphcKARINA ANDRIGHETTI DE OLIVEIRA BRAGA
hcfmusp.contributor.author-fmusphcNATALIA APARECIDA NEPOMUCENO DA SILVA
hcfmusp.contributor.author-fmusphcFABIO BISCEGLI JATENE
hcfmusp.description.beginpage461
hcfmusp.description.endpage469
hcfmusp.description.issue4
hcfmusp.description.volume38
hcfmusp.lim.ref2012
hcfmusp.origemWOS
hcfmusp.origem.pubmed22964930
hcfmusp.origem.scieloSCIELO:S1806-37132012000400008
hcfmusp.origem.scopus2-s2.0-84866356465
hcfmusp.origem.wosWOS:000308281600008
hcfmusp.publisher.cityBRASILIA DF
hcfmusp.publisher.countryBRAZIL
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hcfmusp.scopus.lastupdate2024-04-12
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