Involvement of nitric oxide pathways in neurogenic pulmonary edema induced by vagotomy

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dc.contributor.authorBlanco, Eleonora
dc.contributor.authorMartins-Pinge, Marli
dc.contributor.authorOliveira-Sales, Elizabeth Barbosa de [UNIFESP]
dc.contributor.authorBusnardo, Cristiane
dc.contributor.institutionUniversidade Estadual de Londrina
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionUniversity of São Paulo
dc.date.accessioned2015-06-14T13:42:43Z
dc.date.available2015-06-14T13:42:43Z
dc.date.issued2011-01-01
dc.description.abstractOBJECTIVE: The objective of this study was to evaluate the involvement of peripheral nitric oxide (NO) in vagotomy-induced pulmonary edema by verifying whether the nitric oxide synthases (NOS), constitutive (cNOS) and inducible (iNOS), participate in this mechanism. INTRODUCTION: It has been proposed that vagotomy induces neurogenic pulmonary edema or intensifies the edema of other etiologies. METHODS: Control and vagotomized rats were pretreated with 0.3 mg/kg, 3.0 mg/kg or 39.0 mg/kg of L-NAME, or with 5.0 mg/kg, 10.0 mg/kg or 20.0 mg/kg of aminoguanidine. All animals were observed for 120 minutes. After the animals' death, the trachea was catheterized in order to observe tracheal fluid and to classify the severity of pulmonary edema. The lungs were removed and weighed to evaluate pulmonary weight gain and edema index. RESULTS: Vagotomy promoted pulmonary edema as edema was significantly higher than in the control. This effect was modified by treatment with L-NAME. The highest dose, 39.0 mg/kg, reduced the edema and prolonged the survival of the animals, while at the lowest dose, 0.3 mg/kg, the edema and reduced survival rates were maintained. Aminoguanidine, regardless of the dose inhibited the development of the edema. Its effect was similar to that observed when the highest dose of L-NAME was administered. It may be that the non-selective blockade of cNOS by the highest dose of L-NAME also inhibited the iNOS pathway. CONCLUSION: Our data suggest that iNOS could be directly involved in pulmonary edema induced by vagotomy and cNOS appears to participate as a protector mechanism.en
dc.description.affiliationUniversidade Estadual de Londrina
dc.description.affiliationFederal University of São Paulo
dc.description.affiliationUniversity of São Paulo
dc.description.affiliationUnifespUNIFESP
dc.description.sourceSciELO
dc.format.extent1061-1066
dc.identifierhttp://dx.doi.org/10.1590/S1807-59322011000600024
dc.identifier.citationClinics. Faculdade de Medicina / USP, v. 66, n. 6, p. 1061-1066, 2011.
dc.identifier.doi10.1590/S1807-59322011000600024
dc.identifier.fileS1807-59322011000600024.pdf
dc.identifier.issn1807-5932
dc.identifier.scieloS1807-59322011000600024
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/6131
dc.identifier.wosWOS:000293410000024
dc.language.isoeng
dc.publisherFaculdade de Medicina / USP
dc.relation.ispartofClinics
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectPulmonary Weighten
dc.subjectNitric oxide synthaseen
dc.subjectL-NAMEen
dc.subjectAminoguanidineen
dc.subjectEdema Indexen
dc.titleInvolvement of nitric oxide pathways in neurogenic pulmonary edema induced by vagotomyen
dc.typeinfo:eu-repo/semantics/article
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