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

Detalhes bibliográficos
Autor(a) principal: Blanco, Eleonora
Data de Publicação: 2011
Outros Autores: Martins-Pinge, Marli, Oliveira-Sales, Elizabeth, Busnardo, Cristiane
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Clinics
Texto Completo: https://www.revistas.usp.br/clinics/article/view/19528
Resumo: OBJECTIVE: 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.
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spelling Involvement of nitric oxide pathways in neurogenic pulmonary edema induced by vagotomy Pulmonary WeightNitric oxide synthaseL-NAMEAminoguanidineEdema Index OBJECTIVE: 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. Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo2011-01-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://www.revistas.usp.br/clinics/article/view/1952810.1590/S1807-59322011000600024Clinics; Vol. 66 No. 6 (2011); 1061-1066 Clinics; v. 66 n. 6 (2011); 1061-1066 Clinics; Vol. 66 Núm. 6 (2011); 1061-1066 1980-53221807-5932reponame:Clinicsinstname:Universidade de São Paulo (USP)instacron:USPenghttps://www.revistas.usp.br/clinics/article/view/19528/21591Blanco, EleonoraMartins-Pinge, MarliOliveira-Sales, ElizabethBusnardo, Cristianeinfo:eu-repo/semantics/openAccess2012-05-23T16:46:57Zoai:revistas.usp.br:article/19528Revistahttps://www.revistas.usp.br/clinicsPUBhttps://www.revistas.usp.br/clinics/oai||clinics@hc.fm.usp.br1980-53221807-5932opendoar:2012-05-23T16:46:57Clinics - Universidade de São Paulo (USP)false
dc.title.none.fl_str_mv Involvement of nitric oxide pathways in neurogenic pulmonary edema induced by vagotomy
title Involvement of nitric oxide pathways in neurogenic pulmonary edema induced by vagotomy
spellingShingle Involvement of nitric oxide pathways in neurogenic pulmonary edema induced by vagotomy
Blanco, Eleonora
Pulmonary Weight
Nitric oxide synthase
L-NAME
Aminoguanidine
Edema Index
title_short Involvement of nitric oxide pathways in neurogenic pulmonary edema induced by vagotomy
title_full Involvement of nitric oxide pathways in neurogenic pulmonary edema induced by vagotomy
title_fullStr Involvement of nitric oxide pathways in neurogenic pulmonary edema induced by vagotomy
title_full_unstemmed Involvement of nitric oxide pathways in neurogenic pulmonary edema induced by vagotomy
title_sort Involvement of nitric oxide pathways in neurogenic pulmonary edema induced by vagotomy
author Blanco, Eleonora
author_facet Blanco, Eleonora
Martins-Pinge, Marli
Oliveira-Sales, Elizabeth
Busnardo, Cristiane
author_role author
author2 Martins-Pinge, Marli
Oliveira-Sales, Elizabeth
Busnardo, Cristiane
author2_role author
author
author
dc.contributor.author.fl_str_mv Blanco, Eleonora
Martins-Pinge, Marli
Oliveira-Sales, Elizabeth
Busnardo, Cristiane
dc.subject.por.fl_str_mv Pulmonary Weight
Nitric oxide synthase
L-NAME
Aminoguanidine
Edema Index
topic Pulmonary Weight
Nitric oxide synthase
L-NAME
Aminoguanidine
Edema Index
description OBJECTIVE: 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.
publishDate 2011
dc.date.none.fl_str_mv 2011-01-01
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv https://www.revistas.usp.br/clinics/article/view/19528
10.1590/S1807-59322011000600024
url https://www.revistas.usp.br/clinics/article/view/19528
identifier_str_mv 10.1590/S1807-59322011000600024
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv https://www.revistas.usp.br/clinics/article/view/19528/21591
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo
publisher.none.fl_str_mv Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo
dc.source.none.fl_str_mv Clinics; Vol. 66 No. 6 (2011); 1061-1066
Clinics; v. 66 n. 6 (2011); 1061-1066
Clinics; Vol. 66 Núm. 6 (2011); 1061-1066
1980-5322
1807-5932
reponame:Clinics
instname:Universidade de São Paulo (USP)
instacron:USP
instname_str Universidade de São Paulo (USP)
instacron_str USP
institution USP
reponame_str Clinics
collection Clinics
repository.name.fl_str_mv Clinics - Universidade de São Paulo (USP)
repository.mail.fl_str_mv ||clinics@hc.fm.usp.br
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