Zusammenfassung
Das ausgedehnte Gewebetrauma, Schockereignisse und v.a. bakterielle Infektionen führen nach heutigem Kenntnisstand zur Aktivierung der humoralen Kaskadensysteme: Gerinnungs-/Fibrinolysesystem, Komplementsystem, Kalli-krein-/Kininsystem. Faktoren aus diesen Systemen sind in der Lage, das Sepsis-syndrom mit Organversagen direkt (durch unmittelbare Beeinträchtigung von Zell- und Organfunktionen) oder indirekt durch Aktivierung von Zellsystemen mit konsekutiver Liberierung von Entzündungsmediatoren zu beeinflussen. Dabei sind ganz offensichtlich nicht einzelne Komponenten, sondern vielmehr komplexe Interaktionen zahlreicher Faktoren maßgebend für die Auslösung und Manifestation des septischen Geschehens bis hin zum Organversagen (Abb. 7.1).
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Inthorn, D. (1996). Therapie mit Proteinaseinhibitoren. Antithrombin III. In: Schuster, HP. (eds) Intensivtherapie bei Sepsis und Multiorganversagen. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-07958-4_7
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DOI: https://doi.org/10.1007/978-3-662-07958-4_7
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