Hostname: page-component-78c5997874-g7gxr Total loading time: 0 Render date: 2024-11-16T07:28:07.527Z Has data issue: false hasContentIssue false
  • English
  • Français

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
Get access

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

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Xu H, Gonzalo JA, St Pierre Yet al. Leukocytosis and resistance to septic shock in intercellular adhesion molecule 1-deficient mice. J Exp Med 1994; 180: 95–109.Google Scholar
Carden DL, Young JA, Granger DN. Pulmonary microvascular injury after intestinal ischemia–reperfusion: role of P-selectin. J Appl Physiol 1993; 75: 2529–2534.Google Scholar
Granger DN, Kubes P. The microcirculation and inflammation: modulation of leukocyte–endothelial cell adhesion. J Leukocyte Biol 1994; 55: 662–675.Google Scholar
Marzi I, Knee J, Buhren V, Menger M, Trentz O. Reduction by superoxide dismutase of leukocyte–endothelial adherence after liver transplantation. Surgery 1992; 111: 90–97.Google Scholar
Benkoel L, Dodero F, Hardwigsen Jet al. Expression of intercellular adhesion molecule-1. Digest Dis Sci 2003; 48: 2167–2172.Google Scholar
Lehmkuhl H, Horn C, von der DPet al. Analysis of adhesion molecules in myocardial biopsies of cardiac allografts and coronary artery disease with CABG. J Cardiovasc Surg (Torino) 1996; 37: 65–70.Google Scholar
Lundberg AH, Granger N, Russell Jet al. Temporal correlation of tumor necrosis factor-alpha release, upregulation of pulmonary ICAM-1 and VCAM-1, neutrophil sequestration, and lung injury in diet-induced pancreatitis. J Gastrointest Surg 2000; 4: 248–257.Google Scholar
Sluiter W, Pietersma A, Lamers JM, Koster JF. Leukocyte adhesion molecules on the vascular endothelium: their role in the pathogenesis of cardiovascular disease and the mechanisms underlying their expression. J Cardiovasc Pharmacol 1993; 22 (Suppl 4): S37–S44.Google Scholar
Kalogeris TJ, Kevil CG, Laroux FS, Coe LL, Phifer TJ, Alexander JS. Differential monocyte adhesion and adhesion molecule expression in venous and arterial endothelial cells. Am J Physiol 1999; 276: L9–L19.Google Scholar
Zhang XP, Kelemen SE, Eisen HJ. Quantitative assessment of cell adhesion molecule gene expression in endomyocardial biopsy specimens from cardiac transplant recipients using competitive polymerase chain reaction. Transplantation 2000; 70: 505–513.Google Scholar
Kurose I, Anderson DC, Miyasaka Met al. Molecular determinants of reperfusion-induced leukocyte adhesion and vascular protein leakage. Circ Res 1994; 74: 336–343.Google Scholar
Callicutt CS, Sabek O, Fukatsu Ket al. Diminished lung injury with vascular adhesion molecule-1 blockade in choline-deficient ethionine diet-induced pancreatitis. Surgery 2003; 133: 186–196.Google Scholar
Cominacini L, Garbin U, Fratta PAet al. Lacidipine inhibits the activation of the transcription factor NF-kappaB and the expression of adhesion molecules induced by pro-oxidant signals on endothelial cells. J Hypertens 1997; 15: 1633–1640.Google Scholar
Murphy PG, Myers DS, Davies MJ, Webster NR, Jones JG. The antioxidant potential of propofol (2,6-diisopropylphenol). Br J Anaesth 1992; 68: 613–618.Google Scholar
Musacchio E, Rizzoli V, Bianchi M, Bindoli A, Galzigna L. Antioxidant action of propofol on liver microsomes, mitochondria and brain synaptosomes in the rat. Pharmacol Toxicol 1991; 69: 75–77.Google Scholar
Mathy-Hartert M, Mouithys-Mickalad A, Kohnen S, Deby-Dupont G, Lamy M, Hans P. Effects of propofol on endothelial cells subjected to a peroxynitrite donor (SIN-1). Anaesthesia 2000; 55: 1066–1071.Google Scholar
Jaffe EA, Nachman RL, Becker CG, Minick CR. Culture of human endothelial cells derived from umbilical veins. Identification by morphologic and immunologic criteria. J Clin Invest 1973; 52: 2745–2756.Google Scholar
Gerritsen ME, Carley W, Milici AJ. Microvascular endothelial cells: isolation, identification and cultivation. In: Satovol K, Muramorsch K, eds. Advances in Cell Culture.New York: Academic Press Inc., 1988: 35–67.
Ichikawa H, Flores S, Kvietys PRet al. Molecular mechanisms of anoxia/reoxygenation-induced neutrophil adherence to cultured endothelial cells. Circ Res 1997; 81 (6): 922–931.Google Scholar
Kokura S, Wolf RE, Yoshikawa T, Ichikawa H, Granger DN, Aw TY. Endothelial cells exposed to anoxia/reoxygenation are hyperadhesive to T-lymphocytes: kinetics and molecular mechanisms. Microcirculation 2000; 7: 13–23.Google Scholar
Manning AM, Bell FP, Rosenbloom CLet al. NF-kappa B is activated during acute inflammation in vivo in association with elevated endothelial cell adhesion molecule gene expression and leukocyte recruitment. J Inflamm 1995; 45: 283–296.Google Scholar
Connolly JrES, Winfree CJ, Springer TAet al. Cerebral protection in homozygous null ICAM-1 mice after middle cerebral artery occlusion. Role of neutrophil adhesion in the pathogenesis of stroke. J Clin Invest 1996; 97: 209–216.Google Scholar
Byrne JG, Smith WJ, Murphy MP, Couper GS, Appleyard RF, Cohn LH. Complete prevention of myocardial stunning, contracture, low-reflow, and edema after heart transplantation by blocking neutrophil adhesion molecules during reperfusion. J Thorac Cardiovasc Surg 1992; 104: 1589–1596.Google Scholar
Cominacini L, Garbin U, Fratta PAet al. Lacidipine inhibits the activation of the transcription factor NF-kappaB and the expression of adhesion molecules induced by pro-oxidant signals on endothelial cells. J Hypertens 1997; 15: 1633–1640.Google Scholar
Marik PE. Propofol: an immunomodulating agent. Pharmacotherapy 2005; 25: 28S–33S.Google Scholar
Demiryurek AT, Cinel I, Kahraman Set al. Propofol and intralipid interact with reactive oxygen species: a chemiluminescence study. Br J Anaesth 1998; 80: 649–654.Google Scholar
Kahraman S, Demiryurek AT. Propofol is a peroxynitrite scavenger. Anesth Analg 1997; 84: 1127–1129.Google Scholar