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The uptake of free fatty acids into surface membranes has been shown to affect lymphocyte capping and fibroblast adhesion and growth. Using human gel filtered platelets (GFP), we examined the effects of saturated (S), cis-unsaturated (CU) and trans-unsaturated (TU) fatty acids (FA) on platelet morphology, shape change, aggregation, 5HT release, TxB2 production and diphenyl hexatriene (DPH) polarization, an index of membrane lipid organization. FA (1-30 μM) did not alter platelet morphology. CUFA (16:1, 18:1, 18:2, 18:3, 20:1, 20:2) but not TUFA (18:1, 18:2) or SFA (14:0, 16:0, 18:0, 20:0) inhibited thrombin (T)-induced platelet aggregation and 5HT release. Up to 1514 mninutes after addition of 14C-FA to GFP, &gt;90% of platelet C was present as free FA. Under these conditions only CUFA inhibited T-induced platelet shape change and primary or secondary aggregation induced by ADP, U46619, collagen or arachidonate. Responses to A23187 were unaffected. T-induced TxB2 production was reduced by CUFA. The antiplatelet effects were evident despite the presence of inhibitors of adenylate cyclase (2',5'-dideoxy adenosine, 100μM) or cyclo-oxygenase (indomethacin, 30 μM), but were reversed by resuspension of FA-GFP in FA-free buffer. Analysis of fluorescence decay of DPH in platelet membranes revealed lifetime heterogeneity, indicative of distinct lipid domains. Only CUFA caused a decrease in DPH polarization of intact platelets and platelet membranes. These findings suggest that inhibition of receptor mediated platelet responses by CUFA is produced by perturbation of the platelet membranes in specific lipid domains.

CIS-Unsaturated Fatty Acids Inhibit Platelet Function By Perturbation Of The Platelet Membrane