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Objective: Hypercholesterolemia is an inflammatory disease and a leading cause of atherosclerosis. Platelet hyper-aggregation is observed in hypercholesterolemia and may be mediated by cyclooxygenase (COX) which catalyzes the production of strong inflammatory mediators including thromboxane A2. To understand better the role of COX we measured the antiplatelet effects of the COX-2 inhibitors nimesulide and celecoxib in hypercholesterolemic rabbits. Material and Method: We studied rabbits that consumed a normal diet and three groups maintained on a high cholesterol diet that received saline, nimesulide (25 mg/lzg) or celecoxib (25 mg/kg) for 20 weeks. Blood was obtained from each rabbit every two weeks for measurement of lipid profile by spectrophotometry assay and platelet aggregation-induced by arachidonic acid (AA) and platelet activatxngfactor (PAR, was measured in a Lumi aggregometer. Results: Blood obtained from rabbits fed the high cholesterol diet and receiving only saline treatment showed hyper-aggregation to bothAA and PAF, suggesting that hypercholesterolemia induced pro-aggregatory environment in the blood. Nimesulide showed more than 75% and celecoxib more than 37% inhibition of platelet aggregation induced by both AA and PAF in the two test groups of hypercholesterolemic rabbits. Conclusion: We conclude that the cox inhibitors nimesulide and celecoxib decreased platelet aggregation in hypercholesterolemic rabbits. [ABSTRACT FROM AUTHOR]