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Open Access Research article

Adrenoceptor stimulation does not affect ICAM-1 and VCAM-1 expression in vitro

Heiner Ruschulte1*, Dirk Scheinichen1, Martijn van Griensven2, Susanne Weyrauch1, Wibke Liefing1, Birgitt Harrmeijer1, Michael Przemeck1 and Björn Jüttner1

Author Affiliations

1 Dept. of Anaesthesiology & Intensive Care Medicine, Hannover Medical School Hannover, Germany

2 Department of Trauma Surgery, Hannover Medical School Hannover, Germany

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BMC Research Notes 2011, 4:40  doi:10.1186/1756-0500-4-40

Published: 25 February 2011



Endothelial adhesion molecules ICAM-1 (CD54) and VCAM-1 (CD106) mediate cellular adhesion and transcellular migration. Cell adhesion and diapedesis have a key role in the course of shock and sepsis. During severe sepsis, adrenoceptor agonist levels may be increased due to endogenous production or due to intensive care treatment. As yet, the influence of β1 or β2 agonists on adhesion molecule formation on endothelial cells has remained unclear.


Cultured human umbilical vein endothelial cells were stimulated with E. coli. Following bacterial stimulation the cells were incubated with either β2 receptor agonist terbutaline or β1 agonist norepinephrine. ICAM-1 and VCAM-1 expression were examined using flow cytometry.


Administration of norepinephrine did not cause increases of both CD54 and CD106 in stimulated HUVEC. Compared to negative controls the bacterial stimulation itself led to an increase of adhesion molecules. Following administration of terbutaline no significant increase in CD54 expression was found.


Bacterial stimulation led to an increase of adhesion molecule expression. Adrenoceptor stimulation of activated endothelial cells did not cause significant increases of cellular adhesion molecules.