Hamostaseologie 2005; 25(01): 39-49
DOI: 10.1055/s-0037-1619643
Original Article
Schattauer GmbH

Die zentrale Rolle der Thrombozyten im neuen Verständnis der Hämostase

Platelets and the new comprehension of haemostasis
K. Jurk
1   Experimentelle und Klinische Hämostaseologie, Klinik und Poliklinik für Anästhesiologie und operative Intensivmedizin, Universitätsklinikum Münster
,
B. E. Kehrel
1   Experimentelle und Klinische Hämostaseologie, Klinik und Poliklinik für Anästhesiologie und operative Intensivmedizin, Universitätsklinikum Münster
› Author Affiliations
Further Information

Publication History

Publication Date:
27 December 2017 (online)

Zusammenfassung

Thrombozyten steuern die primäre Hämostase und begrenzen die Gerinnung auf den Ort der Verletzung. Bei einer Gefäßverletzung kommt Blut in Kontakt mit adhäsiven Proteinen des Subendothels und mit Zellen, die konstitutiv TF (tissue factor) exprimieren. Plättchen adhärieren, werden aktiviert, breiten sich aus und setzen Granulainhaltsstoffe frei. Auf der Oberfläche TF-präsentierender Zellen kann nur wenig Thrombin gebildet werden. Diese geringe Thrombinmenge initiiert zwar die Aktivierung zirkulierender Plättchen und der Faktoren XI, VIII und V, reicht aber nicht zur Bildung eines stabilen Thrombus aus. Aktivierte Plättchen aggregieren und assoziieren mit Leukozyten. Die Gerinnungskomplexe binden rezeptorvermittelt an die Plättchenoberfläche, wodurch ein Schutz vor Gerinnungsinhibitoren und eine effiziente Koagulation gewährleistet wird. Dies führt zu massiver Generierung von Thrombin und Bildung eines stabilen Fibrinnetzes. Blutplättchen besitzen autoregulative Mechanismen, die den Aktivierungsprozess negativ beeinflussen. Neben ihrer zentralen Rolle in der Hämostase sind Plättchen essenziell an Prozessen der Entzündung und der innaten Immunabwehr beteiligt.

Summary

Platelets are cells with key function in primary haemostasis. They localise coagulation to the haemostatic thrombus. After injury of the vessel wall blood contacts subendothelial matrix proteins as well as cells constitutively exposing tissue factor (TF). Platelets adhere to the subendothelial matrix, become activated, spread and secrete the contents of their granules. On the surface of the TF exposing cells minute amounts of thrombin are formed. These amounts of thrombin are inadequate to yield in a stable fibrin clot, but activate platelets and factors XI, VIII, V. In that way the consolidation pathway is triggered. Activated platelets aggregate and bind leukocytes. On the surface of the activated platelets coagulation (co)factor complexes are formed and protected in an optimal way. Thus large amounts of prothrombin are converted to thrombin, creating a so-called thrombin burst. This leads to the formation of a stable platelet-fibrin-clot. Platelets are not always prothrombotic. They have their own mechanisms to stop activation processes and thrombus growth. Besides, its key role in haemostasis platelets are involved in inflammation and innative immune defence.

 
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