High-frequency oscillatory ventilation attenuates oxidative lung injury in a rabbit model of acute lung injury

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dc.contributor.authorRonchi, Carlos Fernando [UNESP]
dc.contributor.authorFerreira, Ana Lúcia dos Anjos [UNESP]
dc.contributor.authorCampos, Fabio Joly [UNESP]
dc.contributor.authorKurokawa, Cilmery Suemi [UNESP]
dc.contributor.authorCarpi, Mario Ferreira [UNESP]
dc.contributor.authorde Moraes, Marcos Aurelio [UNESP]
dc.contributor.authorBonatto, Rossano César [UNESP]
dc.contributor.authorFaveri, Julio de [UNESP]
dc.contributor.authorYeum, Kyung-Jin
dc.contributor.authorFioretto, José Roberto [UNESP]
dc.contributor.institutionTufts Univ
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2014-05-20T13:37:30Z
dc.date.available2014-05-20T13:37:30Z
dc.date.issued2011-10-01
dc.description.abstractMechanical ventilation (MV) can induce lung oxidative stress, which plays an important role in pulmonary injury. This study compared protective conventional mechanical ventilation (CMV) and high-frequency oscillatory ventilation (HFOV) for oxygenation, oxidative stress, inflammatory and histopathological lung injury in a rabbit model of acute lung injury (ALI). Rabbits (n = 30) were ventilated at FiO(2) 1.0. Lung injury was induced by tracheal saline infusion (30 mL/kg, 38 degrees C). Animals were randomly assigned to: (a) sham control (CG: tidal volume [V(T)] 6 mL/kg, positive end expiratory pressure [PEEP] 5 cmH(2)O, respiratory rate [RR] 40 ipm); (b) ALI + CMV (CMVG: V(T) 6 mL/kg, PEEP 10 cmH(2)O, RR 40 ipm); or (c) ALI + HFOV (HFG: mean airway pressure [Paw] 14 cmH(2)O, RR 10 Hz) groups. Lung oxidative stress was assessed by total antioxidant performance assay, inflammatory response by the number of polymorphonuclear leukocytes/bronchoalveolar lavage fluid/lung and pulmonary histological damage was quantified by a score. Ventilatory and hemodynamic parameters were recorded every 30 min. Both ALI groups showed worse oxygenation after lung injury induction. After four hours of ventilation, HFG showed better oxygenation (partial pressure of oxygen [PaO(2)] - CG: 465.9 +/- 30.5 = HFG: 399.1 +/- 98.2 > CMVG: 232.7 +/- 104 mmHg, P < 0.05) and inflammatory responses (CMVG: 4.27 +/- 1.50 > HFG: 0.33 +/- 0.20 = CG: 0.16 +/- 0.15; polymorphonuclear cells/bronchoalveolar lavage fluid/lung, P < 0.05), less histopathological injury score (CMVG: 5 [1-16] > HFG: 1 [0-5] > CG: 0 [0-3]; P < 0.05), and lower lung oxidative stress than CMVG (CG: 59.4 +/- 4.52 = HFG: 69.0 +/- 4.99 > CMVG: 47.6 +/- 2.58% protection/g protein, P < 0.05). This study showed that HFOV had an important protective role in ALI. It improved oxygenation, reduced inflammatory process and histopathological damage, and attenuated oxidative lung injury compared with protective CMV under these experimental conditions considering the study limitations.en
dc.description.affiliationTufts Univ, Jean Mayer USDA, Human Nutr Res Ctr Aging, Boston, MA 02111 USA
dc.description.affiliationSão Paulo State Univ UNESP, Botucatu Med Sch, Dept Internal Med, BR-18618970 Botucatu, SP, Brazil
dc.description.affiliationSão Paulo State Univ UNESP, Botucatu Med Sch, Dept Pediat, BR-18618970 Botucatu, SP, Brazil
dc.description.affiliationSão Paulo State Univ UNESP, Botucatu Med Sch, Dept Pathol, BR-18618970 Botucatu, SP, Brazil
dc.description.affiliationUnespSão Paulo State Univ UNESP, Botucatu Med Sch, Dept Internal Med, BR-18618970 Botucatu, SP, Brazil
dc.description.affiliationUnespSão Paulo State Univ UNESP, Botucatu Med Sch, Dept Pediat, BR-18618970 Botucatu, SP, Brazil
dc.description.affiliationUnespSão Paulo State Univ UNESP, Botucatu Med Sch, Dept Pathol, BR-18618970 Botucatu, SP, Brazil
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipUS Department of Agriculture, Agricultural Research Service
dc.description.sponsorshipIdFAPESP: 08/08199-2
dc.description.sponsorshipIdUS USDA: 1950-51000-065-085
dc.format.extent1188-1196
dc.identifierhttp://dx.doi.org/10.1258/ebm.2011.011085
dc.identifier.citationExperimental Biology and Medicine. London: Royal Soc Medicine Press Ltd, v. 236, n. 10, p. 1188-1196, 2011.
dc.identifier.doi10.1258/ebm.2011.011085
dc.identifier.issn1535-3702
dc.identifier.lattes2940051650846541
dc.identifier.lattes8510423269540465
dc.identifier.lattes0246391303241376
dc.identifier.lattes3929692206834380
dc.identifier.orcid0000-0002-0648-876X
dc.identifier.orcid0000-0003-1380-7527
dc.identifier.urihttp://hdl.handle.net/11449/12983
dc.identifier.wosWOS:000296106900012
dc.language.isoeng
dc.publisherRoyal Soc Medicine Press Ltd
dc.relation.ispartofExperimental Biology and Medicine
dc.relation.ispartofjcr2.413
dc.relation.ispartofsjr0,928
dc.rights.accessRightsAcesso restrito
dc.sourceWeb of Science
dc.subjecthigh-frequency oscillatory ventilationen
dc.subjectconventional mechanical ventilationen
dc.subjectacute lung injuryen
dc.subjectoxidative stressen
dc.subjectantioxidantsen
dc.titleHigh-frequency oscillatory ventilation attenuates oxidative lung injury in a rabbit model of acute lung injuryen
dc.typeArtigo
dcterms.licensehttp://www.uk.sagepub.com/aboutus/openaccess.htm
dcterms.rightsHolderRoyal Soc Medicine Press Ltd
unesp.author.lattes2940051650846541[2]
unesp.author.lattes0246391303241376[7]
unesp.author.lattes3929692206834380
unesp.author.lattes8510423269540465[4]
unesp.author.orcid0000-0003-1380-7527[4]
unesp.author.orcid0000-0002-1482-564X[5]
unesp.author.orcid0000-0002-5267-1127[2]
unesp.author.orcid0000-0002-0648-876X[7]
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Medicina, Botucatupt

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