Effects of Inhaled Nitric Oxide on Oxidative Stress and Histopathological and Inflammatory Lung Injury in a Saline-Lavaged Rabbit Model of Acute Lung Injury

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dc.contributor.authorFioretto, José Roberto [UNESP]
dc.contributor.authorCampos, Fabio J.
dc.contributor.authorRonchi, Carlos F. [UNESP]
dc.contributor.authorFerreira, Ana Lúcia dos Anjos [UNESP]
dc.contributor.authorKurokawa, Cilmery Suemi [UNESP]
dc.contributor.authorCarpi, Mario Ferreira [UNESP]
dc.contributor.authorMoraes, Marcos A. [UNESP]
dc.contributor.authorBonatto, Rossano César [UNESP]
dc.contributor.authorFaveri, Julio de [UNESP]
dc.contributor.authorYeum, Kyung-Jin
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.contributor.institutionFaculdade de Medicina de Marília (FAMEMA)
dc.contributor.institutionTufts Univ
dc.date.accessioned2014-05-20T13:37:30Z
dc.date.available2014-05-20T13:37:30Z
dc.date.issued2012-02-01
dc.description.abstractBACKGROUND: Conventional mechanical ventilation (CMV) is fundamental in acute respiratory distress syndrome (ARDS) treatment. Inhaled nitric oxide (INO), an adjunctive therapy, has been used with ventilation in an attempt to improve oxygenation and reduce lung injury. OBJECTIVE: To analyze the early effects of low INO dose on oxygenation, oxidative stress, inflammatory, and histopathological lung injury in a rabbit model of acute lung injury (ALI). METHODS: This was a prospective, controlled, in vivo animal laboratory study. Forty rabbits were instrumented and ventilated at F-IO2 1.0. ALI was induced by tracheal infusion of warm saline (30 mL/kg, 38 degrees C) and lung oxidative stress was assessed by total antioxidant performance (TAP) assay. Animals were assigned to groups: control group (no. = 10, low tidal volume [V-T] = 6 mL/kg, PEEP = 5 cm 1120), ALI without INO (no-INO group, no. = 10, low V-T = 6 mL/kg, PEEP = 10 cm H2O), ALI plus INO (INO group, no. = 10, low V-T = 6 mL/kg, PEEP = 10 cm H2O, INO = 5 ppm). Plateau pressure was limited to 30 cm H2O in all groups. Ten non-instrumented animals (healthy group) were studied for TAP assay. Ventilatory and hemodynamic parameters were recorded every 30 min for 4 hours. RESULTS: After lung injury, the instrumented groups were worse than the control group for P-aO2 (control group 438 +/- 87 mm Hg, no-INO group 80 +/- 13 mm Hg, INO group 81 +/- 24 mm Hg, P < .001). The INO group showed decreased lung inflammation by leukocyte count in lung lavage fluid (no-INO group 4.8 +/- 1.64, control group 0.16 +/- 0.15, INO group 0.96 +/- 0.35 polymorphonuclear cells x 10(6)/bronchoalveolar lavage fluid/lung, P < .001), decreased histopathological injury score (no-INO group 5 [range 1-16], INO group 2 [range 0-5], control group 0 [range 0-3], P < .001), and better lung protection against oxidative injury than the no-INO group (healthy group 68 +/- 8.7, control group 66.4 +/- 6.8, INO group 56.3 +/- 5.1, no-INO group 45.9 +/- 3.4 percent protection/g protein, P < .001). CONCLUSIONS: INO attenuates oxidative stress and histopathological and inflammatory lung injury in a saline-lavaged rabbit ALI model.en
dc.description.affiliationSão Paulo State Univ, Dept Pediat Botucatu, Fac Med Botucatu, BR-18681970 São Paulo, Brazil
dc.description.affiliationSão Paulo State Univ, Dept Internal Med, Fac Med Botucatu, BR-18681970 São Paulo, Brazil
dc.description.affiliationSão Paulo State Univ, Dept Pathol, Fac Med Botucatu, BR-18681970 São Paulo, Brazil
dc.description.affiliationMarilia Med Sch, Marilia, SP, Brazil
dc.description.affiliationTufts Univ, Jean Mayer USDA Human Nutr Res Ctr Aging, Boston, MA 02111 USA
dc.description.affiliationUnespSão Paulo State Univ, Dept Pediat Botucatu, Fac Med Botucatu, BR-18681970 São Paulo, Brazil
dc.description.affiliationUnespSão Paulo State Univ, Dept Internal Med, Fac Med Botucatu, BR-18681970 São Paulo, Brazil
dc.description.affiliationUnespSão Paulo State Univ, Dept Pathol, Fac Med Botucatu, BR-18681970 São Paulo, Brazil
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipIdFAPESP: 07/03173-2
dc.format.extent273-281
dc.identifierhttp://dx.doi.org/10.4187/respcare.01289
dc.identifier.citationRespiratory Care. Irving: Daedalus Enterprises Inc, v. 57, n. 2, p. 273-281, 2012.
dc.identifier.doi10.4187/respcare.01289
dc.identifier.issn0020-1324
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/11449/12982
dc.identifier.wosWOS:000300516700011
dc.language.isoeng
dc.publisherDaedalus Enterprises Inc
dc.relation.ispartofRespiratory Care
dc.relation.ispartofjcr2.073
dc.relation.ispartofsjr0,971
dc.rights.accessRightsAcesso restrito
dc.sourceWeb of Science
dc.subjectARDSen
dc.subjectmechanical ventilationen
dc.subjectoxidative injuryen
dc.subjectacute lung injuryen
dc.subjectrabbitsen
dc.subjectinhaled nitric oxideen
dc.titleEffects of Inhaled Nitric Oxide on Oxidative Stress and Histopathological and Inflammatory Lung Injury in a Saline-Lavaged Rabbit Model of Acute Lung Injuryen
dc.typeArtigo
dcterms.licensehttp://rc.rcjournal.com/site/includefiles/author_information.xhtml#Copyright
dcterms.rightsHolderDaedalus Enterprises Inc
unesp.author.lattes2940051650846541[4]
unesp.author.lattes0246391303241376[8]
unesp.author.lattes3929692206834380
unesp.author.lattes8510423269540465[5]
unesp.author.orcid0000-0003-1380-7527[5]
unesp.author.orcid0000-0002-1482-564X[6]
unesp.author.orcid0000-0002-5267-1127[4]
unesp.author.orcid0000-0002-0648-876X[8]
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Medicina, Botucatupt

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