Key result
Dipyridamole 100 mg t.i.d. for 3 days did not significantly affect platelet content of PDGF or β-TG, nor did it inhibit platelet release of PDGF in healthy volunteers.
Why the study?
Does dipyridamole reduce the platelet release of platelet-derived growth factor in healthy volunteers?
Does dipyridamole reduce the platelet release of platelet-derived growth factor in healthy volunteers?
Dipyridamole does not inhibit the platelet release of PDGF, suggesting that previously reported reductions in serum PDGF levels were likely due to assay interference rather than a true antiplatelet effect.
Dipyridamole does not inhibit platelet PDGF release; challenges prior antiplatelet effect claims and leaves open assay interference as explanation.
Platelet-derived growth factor (PDGF) and β-thromboglobulin (β-TG) are released from platelet alpha-granules during platelet activation. PDGF is a potent chemoattractant and mitogen for human vascular smooth muscle cells, and may be important in the development of late restenosis following angioplasty and in atherogenesis. In recent studies, where PDGF release into serum was evaluated indirectly by measuring (3)H-thymidine incorporation into fibroblasts, it was reported that the antiplatelet drug dipyridamole (DPM) decreased serum levels of PDGF. Such selective inhibition of the PDGF-release would have potential important implications for patients with atherosclerosis and for patients undergoing angioplasty. We therefore measured platelet content of PDGF and β-TG as well as platelet release of PDGF using a newly developed radioimmunoassay in healthy volunteers before and immediately after ingestion of DPM 100 mg t.i.d. for 3 days. We found no significant differences in platelet content of PDGF or β-TG before and after DPM. PDGF release from platelets isolated from plasma by gel filtration and stimulated with thrombin as well as platelet release of PDGF into serum was also unaffected by DPM. In conclusion, treatment with DPM does not affect platelet content of PDGF or β-TG. The treatment did not inhibit the platelet-release of PDGF as previously reported, neither via direct effects on platelets nor on inhibitory plasma components. DPM may, however, inhibit (3)H-thymidine incorporation into fibroblasts.
No takes yet. Share an insight, caveat, or question.
Vissinger et al. (1994) studied Healthy volunteers. Dipyridamole (DPM) vs. Baseline (before ingestion) was evaluated on Platelet content of PDGF and β-TG, and platelet release of PDGF. Dipyridamole 100 mg t.i.d. for 3 days did not significantly affect platelet content of PDGF or β-TG, nor did it inhibit platelet release of PDGF in healthy volunteers.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: