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Provedor de dados:  BJMBR
País:  Brazil
Título:  Pentoxifylline decreases tumor necrosis factor and interleukin-1 during high tidal volume
Autores:  Oliveira-Junior,I.S.
Pinheiro,B.V.
Silva,I.D.C.G.
Salomão,R.
Zollner,R.L.
Beppu,O.S.
Data:  2003-10-01
Ano:  2003
Palavras-chave:  Tumor necrosis factor-alpha
Pentoxifylline
Inflammation
Acute lung injury
Resumo:  Tumor necrosis factor-alpha (TNF-alpha) is one of the most important proinflammatory cytokines which plays a central role in host defense and in the acute inflammatory response related to tissue injury. The major source of TNF-alpha are immune cells such as neutrophils and macrophages. We tested the hypothesis that pentoxifylline, a methylxanthine derivative, down-regulates proinflammatory cytokine expression during acute lung injury in rats. Male Wistar rats weighing 250 to 450 g were anesthetized ip with 50 mg/kg sodium thiopental and randomly divided into three groups: group 1 (N = 7): tidal volume (V T) = 7 ml/kg, respiratory rate (RR) = 50 breaths/min and normal saline infusion; group 2 (N = 7): V T = 42 ml/kg, RR = 9 breaths/min and normal saline infusion; group 3 (N = 7): V T = 42 ml/kg, RR = 9 breaths/min and pentoxifylline infusion. The animals were ventilated with an inspired oxygen fraction of 1.0, a positive end-expiratory pressure of 3 cmH2O, and normal saline or pentoxifylline injected into the left femoral vein. The mRNA of TNF-alpha rapidly increased in the lung tissue within 180 min of ventilation with a higher V T with normal saline infusion. The concentrations of inflammatory mediators were decreased in plasma and bronchoalveolar lavage (BAL) in the presence of higher V T with pentoxifylline infusion (TNF-alpha: plasma, 102.2 ± 90.9 and BAL, 118.2 ± 82.1; IL-1ß: plasma, 45.2 ± 42.7 and BAL, 50.2 ± 34.9, P < 0.05). We conclude that TNF-alpha produced by neutrophil influx may function as an alert signal in host defense to induce production of other inflammatory mediators.
Tipo:  Info:eu-repo/semantics/article
Idioma:  Inglês
Identificador:  http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2003001000011
Editor:  Associação Brasileira de Divulgação Científica
Relação:  10.1590/S0100-879X2003001000011
Formato:  text/html
Fonte:  Brazilian Journal of Medical and Biological Research v.36 n.10 2003
Direitos:  info:eu-repo/semantics/openAccess
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