Potentiation of platelet interaction with collagen substrates by heparin is insensitive to aspirin.

The effects of two standard, unfractionated heparin preparations on collagen-induced adhesion and aggregation of platelets were studied by Born aggregometry and scanning electron microscopy (SEM). Heparin from porcine intestinal mucosa (HI) and from bovine lung (HL) added to human PRP in the concentration of 2.5 to 5.0 U/ml (1) did not induce platelet aggregation in suspension by itself but stimulated it in combination with the subthreshold doses of fibrillar human collagen type III (CIII); (2) increased by 1.5-2.0 fold the adhesion, but did not affect platelet spreading on a surface coated with human collagen type IV (CIV); and (3) enlarged by 2.5-3.0 fold the area of the CIII-coated surface covered with aggregates, increasing both the number and the size of surface-bound aggregates. Aspirin blocked platelet aggregation in suspension induced by low, near threshold doses, of fibrillar CIII and by subthreshold doses of CIII in combination with heparin, but had no effect on platelet aggregation induced by high (greater than 10 threshold) doses of CIII. Aspirin failed to decrease platelet adhesion to and spreading on CIV substrate, and formation of surface-bound aggregates on CIII substrate in the absence as well as in the presence of heparin.