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1908 Part XII Hemostasis and Thrombosis

VIIa IXa Xa

IIa

II
VIIa

Xa F1.2
TF

A Sub-endothelial cell

GPIbα
GPIbα

VIII
PAR1 V PARs

Platelet Activated Platelet
B
IIa

II

VIIa IXa Va Xa F1.2

C Activated Platelet
Fig. 127.2 ASSEMBLY OF THE CRITICAL HEMOSTATIC COMPLEXES OCCURS ON THE
SURFACE OF SUBENDOTHELIAL CELLS AND PLATELETS. (A) All extravascular cell types express
tissue factor (TF) on their surfaces so that clotting is initiated when they come into contact with blood. The
factor VIIa–TF complex can activate factor VII, factor IX and factor X. The factor Xa created at this stage is
thought to activate a small amount of thrombin (IIa) from prothrombin (II). (B) Thrombin can then bind to
the platelets via the receptor GPIbα and cleave protease-activated receptor (PAR) 1 to scramble the membrane
bilayer and expose phosphatidylserine (red surface). The phosphatidylserine-rich surface of the activated platelet
binds the circulating procofactors, factor VIII and factor V with high affinity. Thrombin activates these
cofactors and continues to cleave PARs. (C) Activated platelets now serve as the template for the formation
of the two “engines” of hemostasis, the intrinsic Xase complex (factor VIIIa and factor IXa) and the prothrom-
binase complex (factor Va and factor Xa), leading to the thrombin explosion. (Adapted from Huntington J:
Structural insights into the life history of thrombin. In Tanaka K, Davie E, Ikeda Y, et al, editors: Recent advances in
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thrombosis and hemostasis, Japan, 2008, Springer, p 80–106, with permission.)