Abstract
Sepsis and the systemic inflammatory response syndrome (SIRS) represent an extremely complex biochemical and pathophysiological disorder which still lacks specific effective pharmacological intervention. Infection, trauma, major surgery (e.g., cardiac surgery) or critical illness initiate an inflammatory cascade, which leads to an activation of various regulatory mechanisms. There is a large body of literature implicating that the inflammatory process is initiated and/or maintained by interactions of circulating leukocytes with the endothelium via cell, and organ-specific, adhesion molecules [1–3]. Neutrophils are essential for bacterial killing in infectious disease, but they also are able to injure the host tissue. Neutrophil ‘rolling’ along the endothelium initiates a cascade of cellular interactions resulting in endothelial damage (e.g., capillary leakage) and subsequent development of (multiple) organ damage [3].
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Boldt, J. (2002). Pentoxifylline: A Useful Adjuvant in the Critically Ill?. In: Vincent, JL. (eds) Yearbook of Intensive Care and Emergency Medicine 2002. Yearbook of Intensive Care and Emergency Medicine 2002, vol 2002. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-56011-8_11
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DOI: https://doi.org/10.1007/978-3-642-56011-8_11
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