ABSTRACT
Exposure of mammalian blood to surfaces carrying a negative charge triggers a series of reactions involving activation of the plasma protease zymogens factor XII, factor XI, and plasma prekallikrein (PK), and cleavage of the plasma glycoprotein high-molecularweight kininogen (HK) (Fig. 1) (1-3). These proteins are traditionally referred to as contact factors, and the processes involved in their activation are called contact-activation reactions because a charged surface is needed for them to proceed optimally. Contact activation triggers several host defense mechanisms in vitro, including blood coagulation (Fig. 2) and liberation of vasoactive/proinflammatory kinins from HK (Fig. 1) (1-3). In fact, factors XI (4) and XII (5) were initially identified as missing components of plasma in patients with inherited abnormalities of surface-initiated coagulation. Deficiency of PK (6) or HK (7), components of the kallikrein-kinin system, also causes a defect in surfacemediated coagulation. Despite the clear importance of the contact factors to surfaceinitiated clotting in vitro, a role for contact activation in normal blood coagulation (hemostasis) in vivo appears unlikely.
