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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.

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    Authors
    Corcoran, T B
    Engel, A
    Shorten, G D
    Affiliation
    Cork University Hospital, Department of Anaesthesia, Cork City, Republic of, IrelandUniversity College Cork, Department of Anaesthesia, Cork City, Republic of, Ireland. mascor@gofree.indigo.ie
    Issue Date
    2012-02-03T15:04:51Z
    MeSH
    Analysis of Variance
    Anesthetics, Intravenous/*therapeutic use
    Cell Hypoxia/physiology
    Cells, Cultured
    Endothelial Cells/*drug effects/metabolism
    Endothelium, Vascular/cytology
    Humans
    Intercellular Adhesion Molecule-1/*metabolism
    Leukocytes/immunology
    Oxygen/metabolism
    Propofol/*therapeutic use
    Time Factors
    Umbilical Veins
    Vascular Cell Adhesion Molecule-1/*metabolism
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    Citation
    Eur J Anaesthesiol. 2006 Nov;23(11):942-7. Epub 2006 Jul 11.
    Journal
    European journal of anaesthesiology
    URI
    http://hdl.handle.net/10147/208833
    DOI
    10.1017/S0265021506000846
    PubMed ID
    16834788
    Abstract
    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 microg mL(-1) or propofol 5 microg 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.
    Language
    eng
    ISSN
    0265-0215 (Print)
    0265-0215 (Linking)
    ae974a485f413a2113503eed53cd6c53
    10.1017/S0265021506000846
    Scopus Count
    Collections
    Cork University Hospital

    entitlement

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