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The influence of propofol on the expression of intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) in reoxygenated human umbilical vein endothelial cells

Published online by Cambridge University Press:  11 July 2006

T. B. Corcoran ,
A. Engel  and
G. D. Shorten
T. B. Corcoran
Affiliation:
Cork University Hospital, Department of Anaesthesia, Cork City, Republic of Ireland University College Cork, Department of Anaesthesia, Cork City, Republic of Ireland
A. Engel
Affiliation:
Cork University Hospital, Department of Anaesthesia, Cork City, Republic of Ireland
G. D. Shorten
Affiliation:
Cork University Hospital, Department of Anaesthesia, Cork City, Republic of Ireland University College Cork, Department of Anaesthesia, Cork City, Republic of Ireland
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Abstract

Summary

Background: Leucocytes are a pivotal component of the inflammatory cascade that results in tissue injury in a large group of disorders. Free radical production and endothelial activation promote leucocyte–endothelium interactions via endothelial expression of vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) which augment these processes, particularly in the setting of reperfusion injury. Propofol has antioxidant properties which may attenuate the increased expression of these molecules that is observed. Methods: Cultured human umbilical vein endothelial cells were exposed to 20 h of hypoxia, then returned to normoxic conditions. Cells were treated with saline, Diprivan® 5 μg mL−1 or propofol 5 μg mL−1, for 4 h after reoxygenation and were examined for ICAM-1 and VCAM-1 expression. Results: Hypoxia did not increase the expression of ICAM-1/VCAM-1. ICAM-1 expression peaked 12 h after reoxygenation (21.75(0.6) vs. 9.6(1.3), P = 0.02). Propofol, but not Diprivan®, prevented this increase (8.2(2.9) vs. 21.75(0.6), P = 0.009). VCAM-1 expression peaked 24 h after reoxygenation (9.8(0.9) vs. 6.6(0.6), P = 0.03). Propofol and Diprivan® prevented this increase, with no difference between the two treatments observed (4.3(0.3) and 6.4(0.5) vs. 9.8(0.9), P = 0.001, 0.02, respectively). Conclusion: These effects are likely to be attributable to the antioxidant properties of propofol, and suggest that propofol may have a protective role in disorders where free radical mediated injury promotes leucocyte–endothelium adhesive interactions.

Keywords

LEUCOCYTESENDOTHELIUM VASCULARPROPOFOLFREE RADICALSREPERFUSION INJURYADHESION MOLECULES
Type
Original Article
Information
European Journal of Anaesthesiology , Volume 23 , Issue 11 , November 2006 , pp. 942 - 947
Copyright
2006 European Society of Anaesthesiology

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