Modifications produced by selective inhibitors of cyclooxygenase and ultra low dose aspirin on platelet activity in portal hypertension

doi:10.3748/wjg.v13.i38.5065

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Oct 14, 2007 (publication date) through Apr 20, 2024

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World Journal of Gastroenterology

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1007-9327

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

Basic Research

World J Gastroenterol. Oct 14, 2007; 13(38): 5065-5070
Published online Oct 14, 2007. doi: 10.3748/wjg.v13.i38.5065

Modifications produced by selective inhibitors of cyclooxygenase and ultra low dose aspirin on platelet activity in portal hypertension

Francisco X Eizayaga, Omar Aguejouf, Vanessa Desplat, Philippe Belon, Christian Doutremepuich

Francisco X Eizayaga, CEBBAD, Universidad Maimónides, Buenos Aires, Argentina

Omar Aguejouf, Vanessa Desplat, Christian Doutremepuich, Laboratoire d’Hématologie, Université Victor Segalen, Bordeaux 2, Bordeaux, 146, Rue Léo Saignat, 33076 Bordeaux Cedex, France

Philippe Belon, Laboratoires Boiron, Sainte-Foy-les-Lyons, France

Author contributions: All authors contributed equally to the work.

Correspondence to: Christian Doutremepuich, Laboratoire d’Hématologie, Université Victor Segalen, Bordeaux 2, 146, Rue Léo Saignat, 33076 Bordeaux Cedex, France. christian.doutremepuich@heph.u-bordeaux2.fr

Telephone: +33-5-56987969 Fax: +33-5-56987970

Received: June 6, 2007
Revised: June 21, 2007
Accepted: June 26, 2007
Published online: October 14, 2007

Abstract

AIM: To study the mechanism involved in the potentially beneficial effect of ultra low dose aspirin (ULDA) in prehepatic portal hypertension, rats were pretreated with selective COX 1 or 2 inhibitors (SC-560 or NS-398 respectively), and subsequently injected with ULDA or placebo.

METHODS: Portal hypertension was induced by portal vein ligation. Platelet activity was investigated with an in vivo model of laser induced thrombus production in mesenteric circulation and induced hemorrhagic time (IHT). Platelet aggregation induced by ADP and dosing of prostanoid products 6-keto-PGF_1α, TXB₂, PGE₂ and LTB₄ were also performed.

RESULTS: The portal hypertensive group receiving a placebo showed a decreased in vivo platelet activity with prolonged IHT, an effect that was normalized by ULDA. SC-560 induced a mild antithrombotic effect in the normal rats, and an unmodified effect of ULDA. NS-398 had a mild prothrombotic action in portal hypertensive rats, similar to ULDA, but inhibited a further effect when ULDA was added. An increased 6-keto-PGF_1α was observed in portal hypertensive group that was normalised after ULDA administration. TXA₂ level after ULDA, remained unchanged.

CONCLUSION: These results suggest that the effect of ULDA on platelet activity in portal hypertensive rats, could act through a COX 2 pathway more than the COX 1, predominant for aspirin at higher doses.

Keywords: Ultra Low Dose Aspirin, Portal hypertension, COX 1, COX 2, COX selective inhibition