Abstract
Acute inflammation constitutes the host’s response to a variety of insults, including infection, multiorgan failure associated with sepsis, cancer, trauma, shock, allograft rejection, and ischemia-reperfusion injury. The salient inflammatory reaction that accompanies these states is often related to severe microvascular injury. The consequence of this vascular injury is diffuse endothelial cell damage resulting in 1) increased vascular permeability and extravascular fluid accumulation, 2) enhanced activation of the intrinsic and extrinsic coagulation pathways and inhibition of plasminogen activation favoring a procoagulant state, 3) release of reactive oxygen metabolites, cytokines, vasoactive mediators including kinins, 4) arachidonate metabolites, culminating in augmented intravascular aggregation and transendothelial leukocyte emigration. Although, the principal leukocyte effector cell associated with the above conditions is the neutrophil, other immune and non-immune cells can become active participants in the inflammatory responses. Thus humoral mediators leading to interactions between immune and non-immune cells are important to the full development of the pathogenesis of the acute inflammatory response. In this chapter, we will focus our attention on mediators of inflammation that are potentially critical to the inflammatory response associated with ischemia-reperfusion injury.
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Strieter, R.M. et al. (1993). The Role of Cytokine Networks Mediating Inflammation and Ischemia-Reperfusion Injury. In: Schlag, G., Redl, H., Traber, D. (eds) Shock, Sepsis, and Organ Failure. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-77420-1_8
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DOI: https://doi.org/10.1007/978-3-642-77420-1_8
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