Influence of radiographic contrast media on the secretion of vasoactive substances by primary human umbilical venous endothelial cells (HUVEC): Prospective, controlled, in vitro comparative study
Issue title: Papers from the Regensburg Conference, Regensburg, Germany, 5–6 September 2008
Affiliations: Zentralinstitut für Biomedizinische Technik, Abteilung Biomaterialien, Universität Ulm, Ulm, Germany | GKSS-Forschungszentrum Geesthacht, Berlin–Brandenburg Center for Regenerative Therapies, Campus Virchow-Klinikum der Charité, Universitätsmedizin Berlin, Berlin, Germany
Note: [] Corresponding author: Prof. Dr. F. Jung, Centre for Biomaterial Development, Kantstr. 55, 14513 Teltow, Germany. Tel.: +49 3328 352 269; E-mail: [email protected].
Abstract: Besides the desirable effect of roentgen ray absorption radiographic contrast media (RCM) can also have varying adverse effects. Under discussion, as a possible cause, are microcirculatory disorders resulting from morphological alterations in erythrocytes and endothelial cells. Therefore, the contrast media-induced release of vasoactive substances (prostacyclin, endothelin-1, and nitric oxide (NO)) from human endothelial cells (HUVEC) induced by two commercially available RCMs (Iodixanol 320, Iomeprol 350) was tested in a controlled in-vitro study. The results show that RCMs lead to endothelial cell trauma in vitro, which is apparent in the release of prostacyclin and endothelin-1, while NO release was not affected. The endothelin-1 release after incubation with Iodixanol was similar to the release in the control cultures. In comparison, lower endothelin-1 levels were measured in the cultures incubated with Iomeprol at all 3 time points indicating a more significant cell trauma. Prostacyclin release – also an indicator of traumatization of endothelial cells – increased after addition of both contrast agents. The highest release was found after incubation with Iomeprol 350.
Keywords: Endothelin, prostacyclin, NO, radiographic contrast media, primary human endothelial cells
