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Effects of endothelial cells and mononuclear leukocytes on platelet aggregation

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Although normal vascular endothelium prevents adhesion and aggregation of platelets by the release of nitric oxide (NO) and prostacyclin, the endothelium exposed to oxidized low density lipoprotein (LDL) may be damaged, damage that may include a reduction in its secretory capacity. On the other hand, mononuclear leukocytes (ML) can also release NO to inhibit platelet aggregation. Platelet aggregation was measured with a Chrono-Log aggregometer (USA) in the presence of cultured endothelial cells (EC) or isolated ML, stimulated by collagen. Platelet aggregation was markedly inhibited (28.5±5.0 versus control 92.2±1.7%), when EC were added to platelets. Pre-incubation of the EC with 10 μmol/l of indomethacin or 300 μmol/l of L-NG-monomethyl-arginine (L-NMMA) for 6 h substantially reduced their anti-aggregating activity (72.8±5.1 and 76.6±7.7%, respectively). However, incubation of the EC in culture with 10 μmol/l of lysophosphatidyl choline (LPC) for 6 h did not affect the anti-aggregating capacity of EC (LPC 28.1±5.5 vs. EC 28.5±5.0%). Non-stimulated ML also inhibited (43.2±5.9 vs. control 69.2±3.2%) the platelet aggregation induced by collagen. The inhibition was dependent on the number of ML added. In addition, it was enhanced by increasing the concentration of collagen from 2.5 to 10 μg/ml. Platelet aggregation is inhibited mainly by the EC, however, blood ML also inhibit platelet aggregation. Incubation of the EC in culture with LPC did not affect the anti-aggregating capacity of the EC.


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