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Internal Ca2+ fluxes are known to play a critical role in the activation of human blood platelets as well as for the liberation of arachidonic acid from the phospholipids.  When exogenous arachidonic acid is added to platelets, cyclooxygenase inhibitors, aspirin, flurbiprofen and indo- methacin inhibit its conversion into prostaglandin G2 and H2 and therefore aggregation as well as 14C- serotonin (5-HT) release but they did not affect bovine thrombin - and iono- phore A 23187 induced platelet aggregation and had only little influence on 14C -5 HT release. On the other hand, the intracellular calcium antagonist TMB 8 and chlorpromazine inhibit arachidonic acid-induced platelet aggregation and secretion although they do not affect thromboxane (TX) production. These agents also inhibit platelet aggregation, 14C -5-HT release as well as TX synthesis when ionophore or thrombin are the stimulators. Using a glass capillary column gas chromatography method developed for this purpose, we studied the quantitative amount of the liberated eicosanoids. At high concentrations, TMB 8 and chlorporomazine inhibited strongly arachidonic release as well as platelet aggregation and 14C - 5HT release but although TX production was abolished, arachidonic acid was still liberated and converted to some extent by the lipoxygenase pathway. These findings suggest that internal Ca2+ mobilization is a prerequisite for platelet activation as well as for arachidonic acid liberation. However, at intermediate doses, internal Ca2+ - interfering agents may also modulate the oxidative balance that exists between the cyclooxygenase and the lipoxygenase towards the latter pathway.

Internal Ca2+ Interfering Drugs Alter Arachidonic Acid Metabolism And Inhibit In Vitro Platelet Functions