| Abstract: | Results of our previous study showed that the antihistamine drug cimetidine inhibited functions of blood platelets. The aim of the present paper was to analyse in detail the mechanism of this action. We focussed our attention on the effect of cimetidine on three steps of arachidonic acid metabolism-liberation of arachidonate, biosynthesis of thromboxane A2 and malondialdehyde formation.Cimetidine in the concentration range from 0.01 to 1 mmol/l did not inhibit either thrombin-stimulated liberation of3H-arachidonic acid from individual platelet phospholipids nor malondialdehyde production. Cimetidine at the concentration of 1 mmol/l, however, significantly inhibited the production of thromboxane B2, the stable metabolite of TXA2. |
