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Acta Physiologica Congress

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Acta Physiologica 2007; Volume 190, Supplement 655
XXXIV Congress of The Spanish Society for Physiological Sciences
7/3/2007-7/7/2007
Valladolid, Spain


KETOTIFEN PROPHYLAXIS OF EICOSANOIDS MEDIATED ALTERATIONS IN EXPERIMENTAL PORTAL HYPERTENSION
Abstract number: P84

Nava1 MP, Aller2 MA, Sanchez-Patan2 F, Vara3 E, Garcia3 C, Cuellar4 C, Rodero4 M, Arias2 J

1Complutense University. School of Biology, Department of Physiology (Animal Physiology II)
2School of Medicine, Department of Surgery I
3Department of Biochemistry and Molecular Biology III
4School of Pharmacy. Department of Parasitology`

Intestinal and mesenteric lymph nodes (MLN) infiltration by mast cells is increased in rats with portal hypertension (PHT). The aims of this work are: 1- To demonstrate that hypertensive enteropathy in rats with PHT is due to the release of mediators i.e. eicosanoids by mast cells. 2- To verify that prophylactic Ketotifen administration, a mast cell stabilizer drug, decreases inflammatory alterations related with acute PHT (48 h). Serum Rat Mast Cell Protease (RMCP-II, ELISA) and number of mast cells in ileum and MLN were quantified in pseudo-operated (PSO, n = 12) and portal hypertensive (triple calibration of portal vein stenosis, PHT, n = 12) male Wistar rats. Moreover, serum eicosanoids (RIA) and RMCP-II (ELISA) in ileum and MLN were quantified in four groups of rats receiving vehicle (PSOV, n = 9 and PHTV, n = 10) and Ketotifen (PSOK, n = 10 and PHTK, n = 12) 24 h before surgery.

Serum RMCP-II, Prostaglandin E2 (PGE2) and Leucotrien C4 decrease (p< 0,05) and the number of mast cells and RMCP-II in MLN increase in PHT rats. Ketotifen reduces portal pression (p< 0,05), serum PGE2 (p< 0,001) and RMCP-II (p< 0,001) in MLN. Translocation of mast cells from rat intestinal mucosa to MLN could be a defensive mechanism in acute PHT, avoiding the restoration of an acute intestinal inflammatory response.

To cite this abstract, please use the following information:
Acta Physiologica 2007; Volume 190, Supplement 655 :P84

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