Involvement of nitric oxide pathways in neurogenic pulmonary edema induced by vagotomy
Autor(a) principal: | |
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Data de Publicação: | 2011 |
Outros Autores: | , , |
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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Clinics |
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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 |
_version_ |
1800222757733007360 |