Key result
Heparin improves hemocompatibility over hirudin during extracorporeal circulation, reducing PF4 and C5a activation.
p-value: p=<0.05
Hirudin serves as an alternative anticoagulant for extracorporeal blood circulation. Comparing anticoagulation with hirudin (2.5 or 5.0 microg/mL) and heparin (2.0 or 4.0 IU/mL) human blood was circulated in a modified 'Chandler System' using PVC-tubes for 2 hours at 37 degrees C. Activation of coagulation (thrombin-antithrombin III-complex, prothrombin fragment 1+2 and D-Dimer), platelet (platelet factor 4 - PF4) and complement systems was analyzed. Both heparin concentrations and 5.0 microg/dL hirudin led to as significantly less activated plasmatic coagulation as 2.5 microg/dL hirudin. Decreased levels of PF4 and anaphylatoxin C5a (p<0.05) as well as terminal complement complex demonstrated improved hemocompatibility after anticoagulation with heparin in contrast to hirudin. Because initial coagulation cascade, platelet activation and complement activation is less influenced by hirudin than by heparin, hemocompatibility is more dependent on the characteristics of the biomaterials used. This predestines hirudin as anticoagulant for in vitro studies analyzing hemocompatibility of biomaterials or surface modifications.
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Kopp et al. (2005) studied Extracorporeal blood circulation (in vitro). Hirudin vs. Heparin (2.0 or 4.0 IU/mL) was evaluated on Activation of coagulation, platelet, and complement systems (p=<0.05). Heparin demonstrated improved hemocompatibility compared to hirudin in an in vitro extracorporeal blood circulation model, indicated by decreased levels of PF4 and C5a (p<0.05).
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