SELECTIVE PF4 RELEASE INVITRO INDUCED BY HEPARIN AND RELATED GLYCOSAMINOGLYCANS (GAGS) - CORRELATION WITH BETA-TG RELEASE AND PLATELET-AGGREGATION

Abstract

Human platelet aggregation and .beta.-TG/PF4 [.beta.-thromboglobulin/platelet factor-4] release induced by heparin and related GAG [glycosaminoglycan] in vitro both in normal PRP and in PRP [platelet rich plasma] after aspirin. Heparin and related GAG always caused PF4 release in vitro from normal platelets, whether or not there was measureable platelet aggregation in the aggregometer. Significant .beta.-TG release was induced only by the mucosal heparin preparation (which also induced platelet aggregation in some citrated PRP). While .beta.-TG release in vitro seems to correlate with platelet aggregating activity of heparin, the selective PF4 release, caused by heparin and related GAG also in conditions in which neither platelet aggregation nor .beta.-TG are measureable, is probably associated with the high affinity of PF4 for heparin. The degree of affinity of GAG for PF4 (heparin > DeS [dermatan sulfate] > HS [heparan sulfate]) seems to correlate with PF4 release. The significant reduction in PF4 release in vitro after aspirin suggests that GAG-induced PF4 release is related to a cyclooxygenase-dependent activation process.