Contact-activated coagulation

In vitro studies suggest the albumin is bound in a stable form, possibly involving one or more hydrophobic grooves in the alpha-helical region. The bound albumin may be presented to contact-activating proteins as if it were in bulk form, but one which is not easily desorbed. This treatment is demonstrated, in vivo, to inhibit contact activated coagulation and platelet aggregation. 

Kinins. These hormones are small peptides that induce contraction of smooth muscles, lower blood pressure (Box 22-D), and increase vascular permeability.176 They also have a function in contact-activated blood coagulation. The most important human kinins are the nonapeptide bradykinin177178 and the related decapeptide lysine-bradykinin (Table 30-4). Other forms such as Met-Lys-bradykinin and Ile-Ser-bradykinin (T-kinin) are also known. The precursors to the kinins, the kininogens,176 are cleaved by the protease kallikrein (Fig. 12-17) or by kallikreinlike enzymes to form the kinins. Kinins are suspected of being important producers of pain in inflammatory conditions such as arthritis.1763... 

Pixley FLA, De La Cadena R, Rage J D, et al. The contact system contributes to hypotension but not disseminated intravascular coagulation in lethal bacteremia in vivo use of a monoclonal anti-factor XII antibody to block contact activation in baboons. J Clin Invest 1993 92 61-68. 

Initiation of blood coagulation (clotting) occurs through the contact activation pathway (intrinsic pathway) and the tissue factor (TF) pathway (extrinsic pathway). The contact activation pathway is quantitatively the most important, but is much slower to initiate the TF pathway is considered to be the primary pathway for the initiation of blood coagulation and affords a more rapid response (the so-called thrombin burst), which augments the contact activation pathway. Both pathways share a common pathway that converges at factor X with the production of thrombin (Figure 11.1). 

The coagulation pathway can be activated by one of two pathways the extrinsic (tissue factor) pathway or the intrinsic (contact activation) pathway (Figure 13-1). The main coagulation pathway in vivo is the tissue factor pathway. Tissue factor is exposed by damaged endothelium. This exposed tissue factor binds and activates factor VII, which, in turn, activates factor X. Factor Xa results in the generation of a thrombin (factor lla) burst. Thrombin, in turn activates factors XI, VIII, and V, leading to the further generation of thrombin and clottable fibrin. Additionally, the tissue factor Vila complex activates factor IX, which further contributes to the activation of factor X. 

Shimizu H, Aono K, Masuta K, Asada H, Misaki A, Teraoka H. Degradation of human brain natriuretic peptide (BNP) by contact activation of blood coagulation system. Clin Chim Acta 2001 305 181-6. 

Twelve plasma proteins are considered coagulation factors (Table 100-1). The coagulation factors can be divided into three groups on the basis of biochemical properties. These groups include vitamin K-dependent factors (II, VII, IX, and X), contact activation factors... 

T. Groth, J. Synowitz, G. Malsch, K. Richau, W. Albrecht, K. R Lange and D. Paul, Contact activation of plasmatic coagulation on polymeric membranes measured by the activity of kallilcrein in heparinized plasma Journal of Biomaterials Science Polymer Edition, vol. 8, no. 10, jp. 797-807,1997. 

The test-tube model of coagulation consists of the extrinsic pathway, the intrinsic pathway and a common pathway as shown in Figure 19.3. Damage to a blood vessel exposes TF to the blood, initiating the TF pathway or extrinsic pathway. TF binds zymogen and factor VII to produce activated factor Vila. Factor Vila activates factor X to factor Xa in the common pathway as well as factor IX to factor IXa in the contact activation (intrinsic) path-way,2o.2i jjjjg jg jgygj Qf positive feedback amplification. Activated... 

Both aPTT and PTT measure the coagulation factors of the intrinsic system during a defined activation time until clotting occurs. The difference between both tests resides in the fact that in aPTT kaolin is added to provoke an additional contact activation of factor XII. 

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