Activation of blood coagulation at heparin-coated surfaces

✍ Scribed by Blezer, Ron ;Fouache, Benedicte ;Willems, George M. ;Lindhout, Theo

• Publisher: John Wiley and Sons
• Year: 1997
• Tongue: English
• Weight: 223 KB
• Volume: 37
• Category: Article
• ISSN: 0021-9304
• DOI: 10.1002/(sici)1097-4636(199710)37:1<108::aid-jbm13>3.0.co;2-c

✦ Synopsis

It is hypothesized that immobilized heparin ex-contrast to PU, PU-NAH and PU-HAH are strong mediators erts a dual role in blood coagulation. On the one hand, the of factor XIa and factor IXa formation in normal and antiheparinized surface is because of its dense negative charge, thrombin-deficient plasma. Interestingly, compared to PUthought to initiate the intrinsic pathway of blood coagulation.

HAH and PU-NAH, thrombin formation was only slightly On the other hand, heparin is known as a potent anticoagu-diminished in antithrombin-deficient plasma exposed to PU. lant drug. However, it remains to be seen how much contact-In contrast, thrombin formation was dramatically delayed phase activation of factor XI contributes to thrombin forma-and diminished in normal plasma exposed to PU-HAH. tion and how this process is counterbalanced by which of These findings indicate that very low amounts of factor XIa the anti-protease activities of immobilized heparin. In the apparently suffice to induce significant amounts of thrombin. present study we examined the generation of factors XIa, In this sense, heparinized surfaces are highly thrombogenic, IXa, and Xa, and thrombin in recalcified normal and anti-but our data also indicate that this activity is effectively thrombin-depleted plasma exposed to polyacrylamide-graft counterbalanced by the anti-thrombin activity of the immobipolyurethane (PU) sheets modified by multipoint attachment lized anti-coagulant species of heparin.