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The influence of hyperlipidemic sera on prostacyclin (PGI2) production by cultured endothelial cells was assessed by comparing sera from three types of hyperlipidemias with sera from normal subjects. Sera prepared from normal whole blood (WBS), platelet-rich plasma (PRPS), and platelet-poor plasma (PPPS) were also compared. Bovine aortic endothelial cells (BAEC) incubated with 25% WBS increased PGI2 synthesis significantly within 1 hour, with little further increase by 16 hours; human umbilical vein endothelial cells (HUEC) incubated with 25% WBS for 1 hour showed no elevation in PGI2, whereas PGI2 levels increased substantially after 16 hours. PPPS and PRPS stimulated PGI2 synthesis by BAEC equally at 1 hour. However, there was no rise in PGI2 after PPPS in HUEC; PGI2 rose after 16 hours with PRPS and rose further with WBS after 16 hours. Since WBS best enhanced PGI2 production in human endothelial cells, it was chosen for comparison of the effects of hyperlipidemic and normolipidemic sera. PGI2 synthesis by HUEC significantly increased upon incubation with WBS from Types IIb and IV patients in comparison to WBS from Type IIa hypercholesterolemic patients or normal controls. In contrast, WBS from all these hyperlipidemic subjects stimulated PGI2 synthesis by BAEC similarly to WBS from controls. We conclude that incubation of human endothelial cells with WBS containing high levels of atherogenic lipoproteins does not reduce PGI2 formation by the cells. Moreover, the time course and the contribution of lipid, plasma, or cellular factors to PGI2 formation vary according to the cell type tested. Caution should be exercised in extrapolating results achieved with serum and cells from the same species to other settings.

Prostacyclin production by endothelial cells. Effects of sera from normal and hyperlipidemic subjects.