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Platelet-Derived Growth Factor Release and Antiplatelet Treatment with Low-Dose Acetylsalicylic Acid

University Department of Medicine and Cardiology, Aarhus County Hospital, Aarhus C, Denmark

Steen Elkjaer Husted

University Department of Medicine and Cardiology, Aarhus County Hospital, Aarhus C, Denmark

Steen Dalby Kristensen

University Department of Medicine and Cardiology, Aarhus County Hospital, Aarhus C, Denmark

Hans Kraemmer Nielsen

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)
DOI: 10.1177/000331979304400807


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