Aspirin Reduces Bleeding Severity in Portal Hypertension

Portal hypertension--a major complication of chronic liver disease--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 and dosing of prostanoids were also performed.

Study results showed that the portal hypertensive group receiving a placebo showed a decreased in vivo platelet activity with prolonged IHT, an effect that was normalized by ULDA. ULDA was found to have a normalizing effect on platelet-endothelial cell alterations and bleeding time, an effect mediated by COX 2 inhibition. The authors had no clear explanation to elucidate the effect of such a small dose of aspirin. The study was published in the October 14, 2007, issue of the World Journal of Gastroenterology.

"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,” concluded lead author Professor C. Doutremepuich of the University of Bordeaux 2 and colleagues.

Aspirin is the most widely used antithrombotic agent. Previous research in rats has shown that the prothrombotic properties of ULDA are not mediated by platelets but by endothelial cells, and as such they have the potential of reversing the platelet-endothelial cell interaction alterations observed in portal hypertension. No mechanism has been found to explain this contradictory action.


Related Links:
University of Bordeaux 2
Laboratoires Boiron
Universidad Maimonides