Binding of factor VII to tissue factor (TF) present on or released fro
m cells initiates TF-dependent coagulation in vivo. Earlier data obtai
ned with relipidated TF suspensions led to the hypothesis that all fac
tor VII bound to limiting TF sites exposed after tissue injury could b
e rapidly activated to VIIa/TF complexes by low concentrations of fact
or Xa, IXa, and VIIa. However, newer data on the activation of factor
VII bound to TF expressed on cultured cell monolayers support the hypo
thesis that not all VII/TF complexes formed at a site of tissue injury
are readily activated to VIIa/TF complexes during hemostasis. This is
possibly related to why recombinant factor VIIa can bypass impaired I
Xa/VIIIa/phospholipid complex function in hemostasis.