PLATELET-DERIVED GROWTH-FACTOR RELEASE AND ANTIPLATELET TREATMENT WITH LOW-DOSE ACETYLSALICYLIC-ACID

Platelet-derived growth factor (PDGF) and beta-thromboglobulin (beta-TG) are released from alpha granules during platelet activation. PDGF may play a role in the development of atherosclerosis and the late restenosis after percutaneous transluminal coronary angioplasty (PTCA). The effect of acetylsalicyclic acid (ASA) on PDGF release was studied in healthy volunteers before and twelve hours after ingestion of 300 mg ASA. PDGF, beta-TG, and thromboxane B2(TxB2) were measured by radioimmunoassay (RIA) in serum and in platelet rich plasma (PRP) after submaximal stimulation with collagen. TxB2 decreased significantly from 0.9 +/- 0.3 ng/(mL x 10(6) platelets) to 0.006 +/- 0.005 ng/(mL x 10(6) platelets) (mean +/- SD) in serum after ASA ingestion while PDGF and beta-TG remained unchanged. Measurements in PRP after stimulation with collagen showed a significant decrease in PDGF (from 21.5 +/- 1.4 pg/(mL x 10(6) platelets) to 1.8 +/- 4.1 (pg/mL x 10(6) platelets)), in beta-TG (from 21.0 +/- 13.3 ng/(mL x 10(6) platelets) to 2.2 +/- 1.4 ng/(mL x 10(6) platelets)) and in TxB2 (from 143.6 +/- 80.7 pg/(mL x 10(6) platelets) to 0.5 +/- 0.6 pg/(mL x 10(6) platelets)) after treatment with ASA. In conclusion low-dose ASA inhibits collagen-induced release, of both beta-TG and PDGF in PRP and TxB2-synthesis in PRP and serum.