Enhancement effect of ethanol on lipopolysaccharide-induced procoagulant status in human umbilical endothelial cells.

In spite of the inhibitory effects of ethanol (EtOH) on platelet function, soft blood clots are often observed in cadaveric blood in cases of sudden death after alcohol ingestion. In order to resolve this discrepancy, we have focused on the role of vascular endothelial cells. We tried to investigate the effects of EtOH and LPS on endothelial cells from various perspectives; thrombogenic factor (Von Willebrand factor, VWF), fibrinolytic factor (tissue plasminogen activator, tPA) and inflammatory factor (Interleukin-6, IL-6). Human umbilical vein endothelial cells (HUVECs) were incubated with various concentrations of EtOH (0-160 mM) with or without LPS. Treatment with EtOH and LPS increased VWF release from HUVECs without enhancement mRNA expression. Treatment with 40 mM of EtOH also increased IL-6 release from HUVECs without enhancement mRNA expression. Although EtOH inhibited LPS-induced IL-6 mRNA expression, 20 mM of EtOH still had an increasing effect on the release of IL-6. These doses of EtOH are consistent with a moderate drunkenness level in a normal person. On the other hand, mRNA expression and release reaction of tPA were not affected by EtOH and LPS addition. In conclusion, EtOH enhances procoagulant status via VWF release and IL-6 production cooperation with LPS and may contribute to soft blood clot formation in cadaveric blood.