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Antithrombin–Heparin Complexes
Published in Severian Dumitriu, Valentin Popa, Polymeric Biomaterials, 2020
Leslie R. Berry, Anthony K.C. Chan
Heparin (both UFH and LMWH) provides two major functions in vivo. First, heparin (and other GAGs), mainly in the proteoglycan form, acts as an extracellular matrix component for structural organization and as a chemoattractant in tissue [101,102]. Second, via particular sequences, heparin can operate as anticoagulant. Heparin’s anticoagulant activities are based on its ability to bind to either plasma heparin cofactor II or antithrombin and catalyze their inhibition of thrombin (heparin cofactor II or antithrombin) or other coagulation factors (antithrombin [see earlier]) [103].
Direct Oral Anticoagulants: New Options
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2020
To avoid excessive coagulation, the process is physiologically controlled either by enzyme inhibition or by modulation of the activity of the cofactors (Dahlback, 2000). Tissue factor pathway inhibitor (TFPI) inhibits the initiation of coagulation by forming a complex with FXa, which then binds to TF/FVIIa. The serpin (i.e., serine protease inhibitor) antithrombin (AT) inactivates most of the serine proteases generated during activation of coagulation. The inhibitory potency of this rather slow-reacting inhibitor is enhanced by binding to endothelial heparan sulfate (Alban, 2008a). Similarly, the thrombin inhibitor heparin cofactor II (HCII) is stimulated by binding to glycosaminoglycans.
In Vitro models for thrombogenicity testing of blood-recirculating medical devices
Published in Expert Review of Medical Devices, 2019
In addition to the ISO defined markers in Table 1, studies have also chosen to use less specific means of assessing coagulation: platelet counts, leukocyte counts, partial thromboplastin time (PTT), and gravimetric analysis. Both platelet and leukocyte count are suitable for an overall measure of thrombosis because as they become involved in the clot, they are depleted from serum. Another method that tracks platelet activation is image analysis of adhered platelets on the biomaterial surface [41,53]. Leukocytes are not directly involved in the coagulation cascade, but are integral in regulating key coagulation components. The thrombotic and inflammatory response to biomaterial contact are intricately connected through leukocytes. Engelmann and Massberg coined the phrase ‘immunothrombosis’ to describe the large role that thrombosis plays in innate immune system defense [54]. In addition to their role in the serine-protease conversion of thrombin, leukocytes directly interact with platelets to form platelet-leukocyte aggregates and fibrin to constitute the bulk of the thrombus [55]. A reduction in free leukocyte count due to entrapment in platelet-leukocyte aggregates may be able to provide an overall measure of the innate immune involvement to the blood-recirculating device. In a similar mechanism to platelets, leukocyte subpopulations like neutrophils degranulate after activation within the platelet aggregate and release a variety of chemokines and cytokines that stimulate immune components, such as factors V and VIII in the coagulation cascade [56]. In addition to releasing enzymes with pro-coagulant activity, leukocytes release other enzymes that break down anticoagulant factors such as heparin cofactor II [45].