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Thrombusformation im Blutfluss

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Hämostaseologie

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Zusammenfassung

Physiologischer Schutz gegen Blutung, sogenannte Hämostase, wird durch Plättchenadhäsion und -aggregation an der verletzten Gefäßwand sichergestellt — das Leck wird abgedichtet. Thrombose ist eine hämostatische Reaktion, die fehlgeleitet an einer krankhaft veränderten Gefäßwand abläuft — das Gefäßlumen wird verlegt. Durch den hämodynamischen Vorgang der erythrozytären Axialmigration entsteht im strömenden Blut eine wandnahe Plasmagrenzschicht mit darin angereicherten Thrombozyten, die das Endothel auf Defekte absuchen. Normalerweise nicht im Blut vorhandene Strukturen der Gefäßwand, vor allem Kollagen Typ I und III, triggern das Anhaften der Thrombozyten. Während unter niedrigen Scherraten eine Anzahl von Protein-Rezeptor-Interaktionen möglich ist, bindet unter hohen Scherraten bevorzugt der Plättchenrezeptor Glykoprotein (GP) Ibα an Von-Willebrand-Faktor (vWF), wodurch die schnell strömenden Thrombozyten abgebremst und transient zum Haften gebracht werden. GP Ib benötigt dafür keine Aktivierung.

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Authors and Affiliations

  1. Abt. Transfusionsmedizin/Hämostaseologie, Klinikum der Universität München, Max-Lebsche-Platz 32, D-81377, München

    Prof. Dr. A. J. Reininger

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  1. Prof. Dr. A. J. Reininger
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  1. Institut für Experimentelle Hämatologie und Transfusionsmedizin, Universitätsklinikum Bonn, Sigmund-Freud-Straße 25, 53105, Bonn

    Bernd Pötzsch

  2. Kerckhoff Klinik, BenekeStraße 2-8, 61231, Bad Nauheim

    Katharina Madlener

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Reininger, A.J. (2010). Thrombusformation im Blutfluss. In: Pötzsch, B., Madlener, K. (eds) Hämostaseologie. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-01544-1_9

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  • DOI: https://doi.org/10.1007/978-3-642-01544-1_9

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