| Texto completo | |
| Autor(es): |
Ceron, Carla S.
[1, 2]
;
do Vale, Gabriel T.
[3, 1]
;
Simplicio, Janaina A.
[3, 1]
;
Ricci, Sthefany T.
[1]
;
De Martinis, Bruno S.
[4]
;
de Freitas, Andressa
[5]
;
Tirapelli, Carlos R.
[1]
Número total de Autores: 7
|
| Afiliação do(s) autor(es): | [1] Univ Sao Paulo, Escola Enfermagem Ribeirao Preto, DEPCH, Lab Farmacol, Ribeirao Preto, SP - Brazil
[2] Univ Fed Alfenas, Fac Ciencias Farmaceut, Alfenas, MG - Brazil
[3] Univ Sao Paulo, Fac Med Ribeirao Preto, Programa Posgrad Farmacol, Ribeirao Preto, SP - Brazil
[4] Univ Sao Paulo, Fac Filosofia Ciencias & Letras Ribeirao Preto, Dept Quim, Ribeirao Preto, SP - Brazil
[5] Univ Estadual Londrina, Dept Ciencias Fisiol, Londrina, PR - Brazil
Número total de Afiliações: 5
|
| Tipo de documento: | Artigo Científico |
| Fonte: | European Journal of Pharmacology; v. 825, p. 39-47, APR 15 2018. |
| Citações Web of Science: | 3 |
| Resumo | |
We hypothesized that long-term ethanol consumption would increase the mortality and aggravate the deleterious effects of sub-lethal cecal ligation and puncture (SL-CLP) in the vasculature by inducing the expression of inducible nitric oxide (NO) synthase (iNOS). Male C57BL/6J wild-type (WT) or iNOS-deficient mice (iNOS(-/-)) were treated with ethanol (20% v/v) for 12 weeks and then subjected to SL-CLP. Mice were killed 24 h post-operatively or followed six days for survival. Septic ethanol-treated mice showed a higher mortality than septic WT mice. However, septic iNOS-deficient mice treated with ethanol showed a decreased mortality rate when compared to ethanol-treated WT mice. Ethanol and SL-CLP augmented superoxide anion (O-2(-)) generation in the mesenteric arterial bed (MAB) of both WT and iNOS-deficient mice. Treatment with ethanol and SL-CLP enhanced lipoperoxidation in the MAB of WT, but not iNOS-deficient mice. SL-CLP enhanced nitrate/nitrite (NOx) concentrations in the MAB of WT, but not iNOS-deficient mice. Both, ethanol and SL-CLP increased TNF-alpha and IL-6 levels in the MAB. Treatment with ethanol as well as SL-CLP up-regulated the expression of iNOS in the MAB of WT mice. The major finding of our study is that chronic ethanol consumption increases the mortality induced by SL-CLP and that iNOS plays a role in such response. Although ethanol led to vascular alterations, it did not aggravate the vascular injury induced by SL-CLP. Finally, iNOS mediated the increase in oxidative stress and pro-inflammatory cytokines induced by SL-CLP in the vasculature. (AU) | |
| Processo FAPESP: | 15/22046-8 - Participação dos receptores AT1 no aumento da pressão arterial e do estresse oxidativo vascular induzidos pela abstinência ao etanol |
| Beneficiário: | Carlos Renato Tirapelli |
| Modalidade de apoio: | Auxílio à Pesquisa - Regular |