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

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1. Verfasser: A.B. Alfieri
Format: Artículo científico
Sprache:en
Veröffentlicht: Sociedad Venezolana de Farmacología Clínica y Terapéutica 2004
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author A.B. Alfieri
author_facet A.B. Alfieri
contents 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 A.B. Alfieri L.X. Cubeddu Medicina Radiación Ciclofosfamida Receptores NK1 Glucocorticoides 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 2004 artículo científico 0798-0264 https://www.redalyc.org/articulo.oa?id=55923111 en http://www.redalyc.org/revista.oa?id=559 Archivos Venezolanos de Farmacología y Terapéutica application/pdf Sociedad Venezolana de Farmacología Clínica y Terapéutica Archivos Venezolanos de Farmacología y Terapéutica (República Bolivariana de Venezuela) Num.1 Vol.23
format Artículo científico
id redalyc_55923111
institution Redalyc
language en
publishDate 2004
publisher Sociedad Venezolana de Farmacología Clínica y Terapéutica
spellingShingle 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
A.B. Alfieri
Medicina
Radiación
Ciclofosfamida
Receptores NK1
Glucocorticoides
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 A.B. Alfieri L.X. Cubeddu Medicina Radiación Ciclofosfamida Receptores NK1 Glucocorticoides 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 2004 artículo científico 0798-0264 https://www.redalyc.org/articulo.oa?id=55923111 en http://www.redalyc.org/revista.oa?id=559 Archivos Venezolanos de Farmacología y Terapéutica application/pdf Sociedad Venezolana de Farmacología Clínica y Terapéutica Archivos Venezolanos de Farmacología y Terapéutica (República Bolivariana de Venezuela) Num.1 Vol.23
title 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
topic Medicina
Radiación
Ciclofosfamida
Receptores NK1
Glucocorticoides
url https://www.redalyc.org/articulo.oa?id=55923111