Abstract
Acute inflammation is provoked by a wide variety of mediators. These mediators may affect vascular tone and permeability (e.g. histamine, serotonin), stimulate peripheral pain receptors (e.g. bradykinin), as well as attract and activate inflammatory cells (e.g. complement components, platelet activating factor). The release of mediators from such inflammatory cells (including metabolites of arachidonic acid, lysosomal proteases and oxygen-derived products such as superoxide anion) promote the permanent destructive tissue damage characteristic of the acute inflammatory response.
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Korchak, H.M., Abramson, S.B. (1985). The Role of Arachidonic Acid Metabolites in the Regulation of Neutrophil Function. In: Goodwin, J.S. (eds) Prostaglandins and Immunity. Prostaglandins, Leukotrienes, and Cancer, vol 4. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2603-8_9
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DOI: https://doi.org/10.1007/978-1-4613-2603-8_9
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