Suloctidil, a drug introduced in clinical practice as a vascular antispastic, has been shown to inhibit human platelet aggregation both when added in vitro to PRP and after its oral administration to healthy volunteers. Suloctidil was particularly effective in inhibiting Thrombofax - and collagen - induced aggregation, whereas its inhibitory effect on ADP-induced aggregation was less evident. Neither bleeding time nor platelet retention to glass were modified by suloctidil ingestion. This drug seems therefore to share some properties of both dipyridamole and aspirin-like drugs. However, since in vitro prostaglandin biosynthesis is not inhibited by suloctidil, its inhibitory effect on platelet aggregation could be due to a hitherto unrecognized mechanism of action.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine