Ultra-low-dose aspirin has shown a prothrombotic effect in the laser-induced thrombosis model. Several studies of our laboratory\r\nhave shown a positive effect in rats with two different experimental models of portal hypertension: portal vein ligation, a model\r\nwith an almost normal liver, and 30 days of bile duct ligation, a model with cirrhosis and presence of ascitis. In both models of\r\nportal hypertensive rats, bleeding time was prolonged and thrombi formation, in a laser-induced model of thrombi production,\r\ndecreased. The hypotheses of the presented studies were that ultra-low-dose aspirin could decrease the bleeding complications in\r\nthese models and that the mechanism for these effects could act thorough the COX pathway. In different studies, ultra-low dose\r\nof aspirin normalized the induced hemorrhage time, thrombi production, and platelet-endothelial cell interaction. The possible\r\nbeneficial role of these doses of aspirin and mechanism of COX 2 inhibition are discussed.
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