The Molecular Mechanism of Late Phase Adverse Reaction of Contrast Media

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Endothelial Selectins, such as P-selectin and E-selectin, mediate cell adhesion of monocytes or neutrophils to activated endothelial cells. Previously we reported an upregulated expression of inflammatory cytokines by P-selectin-mediated neutrophil attachment to activated endothelium stimulated by contrast media.We examined the effect of endothelial selectins on the expression of inflammatory cytokines, nitric oxide production and on the activation of NF-kappa B. We found that the soluble forms of P-selectin and E-selectin as well as the monocyte-endothelial interaction induced upregulated the expression of inflammatory cytokines and the production of nitric oxide. These expression of inflammatory cytokines involved the activation of NF-kappa B pathway by the reactive oxygen intermediate (ROI). P-selectin specifically induced β2-integrin (CD11b)-mediated sticky adhesion of monocytes, via ROI generation. Then P-selectin-mediated rapid activation of NF-kappa B, which was augmented by following with β2-integrin (CD11b)-induced sticky adhesion. The binding of endothelial selectins to monocytes in the area of vascular activation by contrast media is considered to be a component of the mechanism that initiates thrombosis and hypotension after the administration of contrast media.