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Mediatorblockade in der Sepsis: Inhibitoren, Antagonisten und Antikörper

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Intensivtherapie bei Sepsis und Multiorganversagen

Zusammenfassung

Gemäß den grundlegenden Ausführungen zur Definition der Sepsis in Kap. 1 steht die systemische Einschwemmung von Mikroben (in der Regel Bakterien oder Pilze) und/oder mikrobiellen Produkten am Anfang der pathophysiologischen Abläufe der Sepsis (Abb. 9-1). Unter den bakteriellen Toxinen haben die Endotoxine gram-negativer Bakterien besondere Beachtung gefunden (Tabelle 9-1). Ihr pathogenetisches Prinzip ist die allen Endotoxinen gemeinsame Lipid-A-Struktur, durch deren beobachtungen am Menschen eine Vielzahl typischer Charakteristika einer Sepsis reproduzieren lassen. Zahlreiche Untersuchungen zur Wirkung des Lipid A haben jedoch gezeigt, daß die meisten (wenn nicht alle) Effekte dieses bakteriellen Agens nicht aus einer „direkt-zytotoxischen“ Wirkung resultieren, sondern mittels Aktivierung körpereigener Mediatorkaskaden und inflammatorisch kompetenter Zellen induziert werden [6, 41].

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Seeger, W., Grimminger, F., Walmrath, D. (2000). Mediatorblockade in der Sepsis: Inhibitoren, Antagonisten und Antikörper. In: Schuster, HP., Werdan, K. (eds) Intensivtherapie bei Sepsis und Multiorganversagen. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-07962-1_9

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  • DOI: https://doi.org/10.1007/978-3-662-07962-1_9

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-662-07963-8

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