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Platelet-Derived Growth Factor Release and Antiplatelet Treatment with Low-Dose Acetylsalicylic AcidUniversity Department of Medicine and Cardiology, Aarhus County Hospital, Aarhus C, Denmark
University Department of Medicine and Cardiology, Aarhus County Hospital, Aarhus C, Denmark
University Department of Medicine and Cardiology, Aarhus County Hospital, Aarhus C, Denmark
University Department of Medicine and Cardiology, Aarhus County Hospital, Aarhus C, Denmark Platelet-derived growth factor (PDGF) and β-thromboglobulin (β-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, β-TG, and thromboxane B2(TxB 2) were measured by radioimmunoassay (RIA) in serum and in platelet rich plasma (PRP) after submaximal stimulation with collagen. TxB2 decreased sig nificantly from 0.9 ± 0.3 ng/(mL x 106 platelets) to 0.006 ± 0.005 ng/(mL x 10 6 platelets) (mean ± SD) in serum after ASA ingestion while PDGF and β-TG remained unchanged. Measurements in PRP after stimulation with collagen showed a significant decrease in PDGF (from 21.5 ± 1.4 pg/(mL x 106 plate lets) to 1.8 ± 4.1 (pg/mL x 106 platelets)), in β-TG (from 21.0 ± 13.3 ng/(mL x 10 6 platelets) to 2.2 ± 1.4 ng/(mL x 106 platelets)) and in TxB2 (from 143.6 ± 80.7 pg/(mL x 106 platelets) to 0.5 ± 0.6 pg/(mL x 106 platelets)) after treat ment with ASA. In conclusion low-dose ASA inhibits collagen-induced release of both β-TG and PDGF in PRP and TxB2-synthesis in PRP and serum.
Angiology, Vol. 44, No. 8,
633-638 (1993) |
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