Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

<jats:p>Several agents inhibit thromboxane synthesis in platelets so might be expected to modulate the arachidonate- induced platelet release reaction and the platelet aggregation that accompanies it. Such agents include the nonsteroidal anti-inflammatory agents (NSAIAs) that inhibit cyclo-oxygenase activity, the selective inhibitor of thromboxane synthetase UK-34787, and dipyridamole. We have assessed their influence on the ability of platelets to convert arachidonate to malondialdehyde (MDA, a marker of thromboxane synthesis) and on the arachidonate-induced release reaction (release of 14C-serotonin from labelled platelets.</jats:p><jats:p>Platelets from different individuals respond differently to some of these agents. Whereas similar concentrations of each of acetylsalicylic acid, indomethacin, flurbiprofen and tolmetin were required to inhibit MDA production in platelets from different donors, higher concentrations of these NSAIAs were sometimes required to inhibit the arachidonate-induced release reaction in platelets from some donors than were required in platelets from others. UK-34787 inhibited both MDA production and the release reaction in platelets from some donors, but in platelets from others it had little effect on release despite inhibiting MDA generation. Dipyridamole was more effective as an inhibitor of the platelet release reaction in platelets that were responsive to UK-34787 than in platelets that were not.</jats:p><jats:p>These different effects of agents on platelets from different individuals might be relevant to their effectiveness in thromboembolic disease. Perhaps participants in clinical trials should be stratified according to the responsiveness of their platelets to the particular drugs under scrutiny.</jats:p>

Original publication




Journal article


Oral Presentations


Schattauer GmbH

Publication Date