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

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

Autor Blanco, Eleonora Google Scholar
Martins-Pinge, Marli Google Scholar
Oliveira-Sales, Elizabeth Barbosa de Autor UNIFESP Google Scholar
Busnardo, Cristiane Google Scholar
Instituição Universidade Estadual de Londrina
Universidade Federal de São Paulo (UNIFESP)
University of São Paulo
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.
Palavra-chave Pulmonary Weight
Nitric oxide synthase
L-NAME
Aminoguanidine
Edema Index
Idioma Inglês
Data de publicação 2011-01-01
Publicado em Clinics. Faculdade de Medicina / USP, v. 66, n. 6, p. 1061-1066, 2011.
ISSN 1807-5932 (Sherpa/Romeo, fator de impacto)
Publicador Faculdade de Medicina / USP
Extensão 1061-1066
Fonte http://dx.doi.org/10.1590/S1807-59322011000600024
Direito de acesso Acesso aberto Open Access
Tipo Artigo
Web of Science WOS:000293410000024
SciELO S1807-59322011000600024 (estatísticas na SciELO)
Endereço permanente http://repositorio.unifesp.br/handle/11600/6131

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