Cilostazol significantly reduced platelet thrombus formation on injured arterial walls, decreasing thrombi coverage from 5.0% in the control group to 0.3% at a concentration of 10^-4 M (p<0.01).
Does cilostazol inhibit platelet thrombus formation and beta-TG release on injured arterial walls in a preclinical model?
Cilostazol inhibits platelet thrombus formation and activation on injured arterial walls without preventing initial platelet adhesion, suggesting a favorable anti-thrombotic profile.
Absolute Event Rate: 0.3% vs 5%
p-value: p=<0.01
Cilostazol was developed as a drug for reducing platelet function. The transformation of platelets on injured arterial wall is very important as a trigger of thrombus formation and creation of structural change of the arterial wall. We investigated the inhibitory effect of cilostazol on platelet adhesion using the Baumgartner's method.In this method, circulating blood through the injured arterial wall was treated with cilostazol (10-3, 10-4, 10-5M) dissolved in N, N-dimethylformamid (DMF) (0.8%). The number of adherent platelets on subendothelium and their forms (spread, contact, thrombi) were studied under light microscopy. Adherent platelets were also studied morphologically by a scanning electron microscope. The localization of β-TG in adherent platelets was studied using the ABC method.Cilostazol reduced ‘thrombi’, but it exerted no effect on the ‘spread’ and increased the ‘contact’ platelets. On scanning electron microscopy, cilostazol also showed the reduction in platelet thrombus formation.β-TG release from platelets seemes to be suppressed by cilostazol at the concentration of 10-4M or above. Cilostazol seems to have the inhibitory effect on platelet thrombus formation, β-TG release and the transfomation from contact to spread.
Ohga et al. (Sun,) conducted a other in Platelet adhesion and thrombus formation. Cilostazol vs. 0.8% N,N-dimethylformamide (DMF) was evaluated on Percentage of subendothelial surface covered with platelet thrombi (p=<0.01). Cilostazol significantly reduced platelet thrombus formation on injured arterial walls, decreasing thrombi coverage from 5.0% in the control group to 0.3% at a concentration of 10^-4 M (p<0.01).