Resumen

ALFIERI, AB  y  CUBEDDU, LX. Efectos de los Antagonistas de los Receptores NK₁ y de la Dexametasona sobre la inflamación neurogénica inducida por ciclofosfamida y por radiación X, en la rata. AVFT [online]. 2004, vol.23, n.1, pp.61-66. ISSN 0798-0264.

The antineoplastic agents cyclophosphamide (CFM) and radiation X (RAD) can produce neurogenic inflammation in the urinary bladder and in the gastrointestinal tract, respectively. NK₁ receptor- antagonists reduce plasma protein extravasation (EPP) caused by diverse antineoplastic drugs; and glucocorticoids increase the efficacy of agents used to treat adverse effects of anti-cancer treatments. In this study we determined whether dexametasone (DEX) modifies the efficacy of NK₁ antagonists to inhibit the EPP induced by CFM or RAD. Male rats received one of the following treatments: saline (1 ml/kg), GR203040 (0.3 mg/kg), GR205171 (0.3 mg/kg), DEX (1mg/kg) or the combination of antagonists NK₁+DEX, before the administration of CFM or RAD. Cytotoxicity in different tissues (bladder, duodenum, jejune and kidney) was determined by quantification of EPP by the Evan’s blue method and by histological evaluation. The individual pre-treatments with a GR or DEX significantly inhibited the EPP induced by CFM in the bladder and by RAD in duodenum and jejune; and that this inhibition was increased when the combination of a GR+DEX was used. The results suggest that both NK₁ receptors and steroid-sensitive mechanisms are involved in CFM or RAD-induced inflammation.

Palabras clave : Cyclophosphamide; Radiation; NK₁ Receptors; Glucocorticoid.