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Human blood platelet behaviour after inhibition of thromboxane synthetase.
Author(s) -
Heptinstall S,
Fox SC
Publication year - 1983
Publication title -
british journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.216
H-Index - 146
eISSN - 1365-2125
pISSN - 0306-5251
DOI - 10.1111/j.1365-2125.1983.tb02104.x
Subject(s) - platelet , thromboxane a2 , thromboxane , chemistry , platelet rich plasma , thromboxane b2 , platelet activation , malondialdehyde , thromboxane a synthase , medicine , pharmacology , endocrinology , biochemistry , oxidative stress
1 We have determined the extent to which sodium arachidonate (NaAA) induces a release reaction in platelet‐rich plasma (PRP) from different individuals and have studied the ability of the thromboxane synthetase inhibitor UK 34787 to modify this release. We have also determined the extent of the platelet release reaction induced in PRP from different individuals by preparations of platelet‐derived thromboxane A2 (TXA2). 2 The release of [14C]‐serotonin induced by NaAA is more extensive in PRP from some individuals than from others. 3 There is a direct relation between the extent of the release reaction induced in different PRPs by NaAA and TXA2. 4 UK 34787 prevents the NaAA‐induced release reaction in PRP from some individuals (“responders”) but not in PRP from others (“non‐responders”). 5 The mean extent of the NaAA‐ induced release reaction for the “non‐responders” was significantly higher than that for the “responders” even in the absence of UK 34787, but there was some overlap between the individual results. 6 Platelets from “responders” and “non‐responders” did not differ in the amount of malondialdehyde (MDA) produced or in the effectiveness with which UK 34787 inhibited MDA production. 7 Platelet‐derived TXA2 from “responders” and “non‐responders” did not have markedly different effects when tested in a single preparation of PRP.