Abstract
Ischemia, which is a marked reduction in blood flow to a vacular bed, can lead to tissue injury and organ dysfunction if it is prolonged. While early restoration of blood flow (reperfusion) to an ischemie organ is essential for prevention of hypox-ic injury, there appears to be a distinct process of vascular dysfunction and parenchymal cell necrosis that can result from this abrupt reperfusion of ischemic tissues. This phenomenon, called “reperfusion injury”, appears to be linked to the reintroduction of molecular oxygen and eventual recruitment of inflammatory cells into postischemic tissues. The importance of activated leukocytes in reperfusion injury is supported by several lines of evidence: (a) leukocytes accumulate in the postischemic tissues, (b) depletion of circulating leukocytes reduces reperfusion-induced tissue injury and “capillary no-reflow”, (c) reagents that interfere with reperfusion-induced leukocyte-endothelial cell adhesion are also effective in blunting the micro vascular dysfunction and tissue injury elicited by ischemia/reperfusion (I/R), (d) reperfusion-induced tissue injury is attenuated in animals that are genetically deficient in adhesion glycoproteins, (e) conditions that exacerbate the inflammatory responses to I/R, such as diabetes and hypercholesterolemia also lead to an enhancement of I/R-induced tissue injury, and (f) I/R-induced inflammatory responses (leukocyte adhesion, increased vascular permeability) can be mimicked in vitro by exposing endothelial cell monolayers to hypoxia and reoxygenation [1-5].
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Aw, T.Y., Granger, D.N. (1999). Control of leukocyte adhesion and activation in ischemiareperfusion injury. In: Pearson, J.D. (eds) Vascular Adhesion Molecules and Inflammation. Progress in Inflammation Research. Birkhäuser, Basel. https://doi.org/10.1007/978-3-0348-8743-4_12
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DOI: https://doi.org/10.1007/978-3-0348-8743-4_12
Publisher Name: Birkhäuser, Basel
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