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Endothelial Cell Dysfunction and Abnormal Tissue Perfusion

  • Chapter
Mechanisms of Organ Dysfunction in Critical Illness

Part of the book series: Update in Intensive Care and Emergency Medicine ((UICMSOFT,volume 38))

Abstract

The vascular endothelium is a highly specialized tissue involved in modulating immune responses and vascular cell growth, and in regulating the level of hemostatic, inflammatory, and vasoactive agents in the blood (Table 1). Endothelial cells line vessels in every organ system and regulate the flow of nutrient substances, diverse biologically active molecules, and the blood cells themselves. This ‘gate-keeping’ role of the endothelium is effected through the presence of membrane-bound receptors for numerous molecules including proteins, lipid transporting particles, metabolites and hormones, as well as through specific junction proteins and receptors that govern cell-to-cell and cell-tomatrix interactions [1]. This feature explains why endothelium dysfunction and/or injury with subendothelium exposure facilitates leukocyte and platelet aggregation and aggravation of coagulopathy. Therefore, endothelial dysfunction and/or injury should favor impaired perfusion, tissue hypoxia and subsequent organ dysfunction.

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Authors and Affiliations

  1. Department of Anesthesiology and Intensive Care, University Hospital of Lille, Rue Michel Polonovski, 59037, Lille Cedex, France

    B. Vallet, E. Wiel & P.-A. Rodie-Talbère

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  2. E. Wiel
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  3. P.-A. Rodie-Talbère
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  1. Intensive Care Unit, Royal Brompton Hospital, Sydney Street, London, SW3 6NP, UK

    Timothy W. Evans

  2. Division of Critical Care Medicine, University of Pittsburgh Medical Center, Scaife Hall, Room 606, 3550 Terrace Street, Pittsburgh, PA, 15264, USA

    Mitchell P. Fink

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Vallet, B., Wiel, E., Rodie-Talbère, PA. (2002). Endothelial Cell Dysfunction and Abnormal Tissue Perfusion. In: Evans, T.W., Fink, M.P. (eds) Mechanisms of Organ Dysfunction in Critical Illness. Update in Intensive Care and Emergency Medicine, vol 38. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-56107-8_12

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