Science

Very low dose aspirin may lessen bleeding in portal hypertension

Last Updated: 2007-11-06 17:23:25 -0400 (Reuters Health)

NEW YORK (Reuters Health) - Findings in a murine model of portal hypertension suggest that the normalizing effect on platelet and endothelial cell activity seen following ultra low-dose aspirin (ULDA) administration may be mediated primarily through the COX 2 pathway.

In the October 14th issue of the World Journal of Gastroenterology, Dr. Christian Doutremepuich and colleagues note that this is in contrast to the antithrombotic effect of higher doses of aspirin, which predominantly involves inhibition of the COX 1 pathway.

Dr. Doutremepuich of Universite Victor Segalen, Bordeaux, France and his team add that ULDA has demonstrated a potentially beneficial effect in animals with portal hypertension by normalizing altered platelet activity and induced hemorrhagic time.

To investigate underlying mechanisms, the researchers studied the effect of ULDA in rats with induced portal hypertension and animals that had undergone a sham procedure, after they were pretreated with a COX 1 inhibitor or a COX 2 inhibitor.

Although the investigators observe that the complex interactions such as vascular responsiveness could not be evaluated, the prothrombotic effect of ULDA was confirmed in animals with and without portal hypertension.

This, the researchers note, was underscored by findings that use of the COX 2 inhibitor induced a mild prothrombotic effect in the rats with portal hypertension, similar to that seen following ULDA alone. Moreover, addition of ULDA to animals already dosed with the COX 2 inhibitor produced no further effect.

This study, Dr. Doutremepuich told Reuters Health, shows the possibility of using the ULDA effect therapeutically.

World J Gastroenterol 2007;13:5065-5070.