Effect of fibrinogen

Nham, S. U., and Fuller, G. M. (1986). Effect of fibrinogen degradation products on production of hepatocyte stimulating factor by a macrophage cell line (P388D1). Thromb. Res. 44, 467-475. 

Senior RM, Skogen Wp Griffin GL, Wilner GD. Effects of fibrinogen derivatives upon the inflammatory response. J Clin Invest 1986 77 1014-1021. 

Cross MX Effect of fibrinogen on the aggregation of platelets by adenosine diphosphate. Thromb Dialfa Haemonh 1964 12 524-527. 

Heparin inhibits the formation of fibrin clots, inhibits the conversion of fibrinogen to fibrin, and inactivates several of the factors necessary for the clotting of blood. Heparin cannot be taken orally because it is inactivated by gastric acid in the stomach therefore, it must be given by injection. Heparin has no effect on clots that have already formed and aids only in preventing the formation of new blood clots (thrombi). The LMWHs act to inhibit clotting reactions by binding to antithrombin HI, which inhibits the synthesis of factor Xa and the formation of thrombin. 

Schmaier AH. Silver L. Adams AL, Fischer GC, Munoz PC, Vroman L, et al The effect of high molecular weight kininogen on surface-adsorbed fibrinogen. Thromb Res 1984 33 51-67. 

A number of laboratory tests are available to measure the phases of hemostasis described above. The tests include platelet count, bleeding time, activated partial thromboplastin time (aPTT or PTT), prothrombin time (PT), thrombin time (TT), concentration of fibrinogen, fibrin clot stabifity, and measurement of fibrin degradation products. The platelet count quantitates the number of platelets, and the bleeding time is an overall test of platelet function. aPTT is a measure of the intrinsic pathway and PT of the extrinsic pathway. PT is used to measure the effectiveness of oral anticoagulants such as warfarin, and aPTT is used to monitor heparin therapy. The reader is referred to a textbook of hematology for a discussion of these tests. 

This drug is more potent and more selective for fibrin-bound plasminogen than any other known plasminogen activator. Unlike t-PA, desmoteplase is not activated by fibrinogen or (3-amyloid proteins, factors that may exacerbate the risk for ICH. Moreover, desmoteplase inhibits t-PA-induced potentiation of excitotoxic injury. The effect of IV administration of desmoteplase 3-9 hours after symptom onset in stroke patients who demonstrate a mismatch on PWI/DWI MRI is currently being investigated. ... 

Ginseng Rg2 has shown inhibitory effects on platelet aggregation similar to aspirin, and R0 reportedly inhibits the conversion of fibrinogen to fibrin [27]. The amount of ginseng administered may also influence the effect(s) produced. In rats and mice, small doses of ginseng extract result in increased spontaneous motor activity, whereas larger doses produce an inhibitory effect on the central nervous system [28]. 

The effects of Lp(a) on the fibrinolytic system are based on the homology between plasminogen and Lp(a) (E3, E5, K4). Inactive Glu-plasminogen is converted to inactive glutamine-plasmin or inactive lysine-plasmin. Both can be converted to active lysine-plasmin, the activity of which is based on the serine protease part that splits fibrin and fibrinogen, but also factors V and Villa. In addition, Lp(a) is able to activate factor XII, factor VII, and the complement factors Cl and C3. 

M19. Matsunaga, A., Handa, K., Mori, T., Moryama, K., Hidaka, K., Yuki, M., Sasaki, J., and Arakawa, K., Effects of nieritrol on levels of serum lipids, lipoprotein(a) and fibrinogen in patients with primary hypercholesterolemia. Atherosclerosis [Pg.126]

Mechanism of Action A glycoprotein Ilb/IIIa receptor inhibitor that rapidly inhibits platelet aggregation by preventing the binding of fibrinogen to GP Ilb/IIIa receptor sites on platelets. Therapeutic Effect Prevents closure of treated coronary arteries. Prevents acute cardiac ischemic complications. 

Mechanism of Action An antiplatelet and antithrombotic agent that binds to platelet receptorglycoproteinllb/Illa, preventing binding of fibrinogen. Therapeutic Effect inhibits platelet aggregation and thrombus formation. 

As for the effect of anionic group, there are a number of reports dealing with the antithrombogenic behavior of sulfonate-modified surfaces of segmented polyurethane (SPU). An interesting feature of the adsorptive behavior of fibrinogen on these material surfaces will be discussed in Sect. 4.1. 

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