Thrombin-induced clot formation

I.M.l In vitro Tests 256 I.M.3.5 Thrombin-Induced Clot Formation... 

Thrombin-Induced Clot Formation in Canine Coronary Artery... 

Some snake venoms, especially from Crotalidae and Viperidae, produce fibrin clots very similar to those produced by thrombin. Such clot formation induces thrombosis in any part of the body. Vasospasm and microcirculation obstruction by fibrin clots contribute to decreased renal blood flow and subsequent decreased urine outflow. These effects are generally transient, since the clots are lysed rapidly and metabolized in vivo. 

Figure 51-5. Formation of a fibrin clot. A Thrombin-induced cleavage of Arg-Gly bonds of the Aaand B(3 chains of fibrinogen to produce fi-brinopeptides (left-hand side) and the a and p chains of fibrin monomer (right-hand side). B Cross-linking of fibrin molecules by activated factor XIII (factor Xllla).

Fibrinogen is a highly water soluble protein present in blood that is responsible for (and the primary component of) trauma-induced blood clots. Clot formation occurs via a thrombin-catalyzed conversion of fibrinogen to fibrin, with subsequent polymerization and cross-linking of fibrin mono-... 

Fibrinogen extravasation Soluble 340 kDa plasma glycoprotein synthesized by hepatocytes and converted by thrombin into fibrin during blood clot formation Fibrinogen extravasation into the nervous tissue can be used as a marker of altered vascular permeability Experimental brain ischemia, injection of hyperosmolar solutions [41 ], hypertension-induced injury [40], toxic brain insult, hmnan cerebral malaria [42], patients with mitochondrial DNA disease [38], AD [43]... 

Platelets can be activated by a variety of agents including the physiologic agonists ADP, thromboxane A2, epinephrine, collagen, and thrombin. Platelet activation is generally associated with a change in platelet shape (except for epinephrine-induced platelet activation) from discs to spiny spheres with pseudopodia. Platelet pseudopod formation is dependent on actin polymerization in the activated platelets. The interaction of actin filaments with myosin, mediated by calcium (9), facilitates platelet contractile activity (e.g., clot retraction). 

Heparin binds to antithrombin III and induces a conformational change that accelerates the interaction of antithrombin III with the coagulation factors. Heparin also catalyzes the inhibition of thrombin by heparin cofactor II, a circulating inhibitor. Smaller amounts of heparin are needed to prevent the formation of free thrombin than are needed to inhibit the protease activity of clot-bound thrombin. Inhibition of free thrombin is the basis of low-dose prophylactic therapy. 

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