Deposition of Platelets on Collagen as Evaluated by ⁵¹Cr-Label or Morphometry: Effects of Aspirin

Whether aspirin inhibits platelet deposition on thrombogenic surfaces by its effect on adhesion-induced aggregation only or whether it also affects adhesion per se, is still controversial. This study compares platelet deposition determined from the deposited radioactivity using ⁵¹Cr-labeled platelets with platelet surface interaction as measured’by morphometry. Collagen fibrils of α-chymotrypsin-digested segments of rabbit aorta were exposed to citrated rabbit blood for 10 min in a perfusion chamber at 830 s^-1 blood shear rate. The number (L) of deposited platelets as calculated from the ⁵¹cr-label amounted to 687±87x10³/mm² (mean ± SE of 35 control perfusions). The surface area covered with platelets (D) as determined by morphometry amounted to 31±2 % and that covered by platelet thrombi (T) (aggregates higher than 5 um) to 19±2 %. The deposited platelet mass (M) as measured by the sum of platelet cross section area multiplied by section thickness amounted to 564±66 μm³/mm². Linear regression analysis showed platelet mass as determined by L and M to be highly correlated (R = 0.9509, 2p (0. 001). Thus platelet deposition on thrombogenic surfaces may be adequately measured by adding a small proportion (l3±1 %) of ⁵¹Cr -labeled homologous platelets to citrated blood.

Aspirin (100 μM) significantly inhibited platelet deposition as shown by decreased values of L, M and T but did not decrease the surface area covered with platelets (D) as evaluated morpho-metrically. Thus the inhibition of platelet deposition on thrombogenic surfaces exerted by aspirin appears to be due to inhibition of a platelet reaction subsequent to adhesion.