Pentoxifylline decreases tumor necrosis factor and interleukin-1 during high tidal volume
Braz. j. med. biol. res
; 36(10): 1349-1357, Oct. 2003. ilus, tab
Article
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| LILACS
| ID: lil-346496
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BR1.1
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
Texto completo:
1
Índice:
LILACS
Asunto principal:
Pentoxifilina
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Inhibidores de Fosfodiesterasa
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Síndrome de Dificultad Respiratoria
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Interleucina-1
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Factor de Necrosis Tumoral alfa
Límite:
Animals
Idioma:
En
Revista:
Braz. j. med. biol. res
Asunto de la revista:
BIOLOGIA
/
MEDICINA
Año:
2003
Tipo del documento:
Article