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

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Abstract

The syndrome of acute lung injury (ALI), known in its most severe form as the acute respiratory distress syndrome (ARDS), is characterized by increased alveolar-capillary membrane permeability and subsequent pulmonary edema. ARDS can be initiated by any one of an extensive and heterogeneous list of pulmonary or systemic insults (Fig. 1), the most frequent of which is sepsis [1]. What these inciting factors have in common, is the ability to initiate activation of an acute inflammatory response, leading to dysfunction of multiple organs including the lung, heart, kidneys, and liver. Polymorphonuclear leukocytes (PMN, neutrophils), that normally pass through the microcirculation of the lung and other tissues relatively unimpeded, are sequestered and activated in the microvasculature during the genesis of an inflammatory response. The activation of neutrophils leads to the release of cytotoxic products that, when released in an unregulated manner, may damage cells in proximity, leading to organ injury and dysfunction.

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Lee, W.L., Downey, G.P. (2002). Role of Leukocytes in Sepsis and Lung Injury. 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_6

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  • DOI: https://doi.org/10.1007/978-3-642-56107-8_6

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