Thrombogenicity of polysaccharide-coated surfaces

被引:59
作者
Keuren, JFW
Wielders, SJH
Willems, GM
Morra, M
Cahalan, L
Cahalan, P
Lindhout, T
机构
[1] Maastricht Univ, Dept Biochem, NL-6200 MD Maastricht, Netherlands
[2] Percardia Inc, Merrimack, NH USA
[3] Nobil Bio Ric, I-14018 Villafranca Dasti, Italy
[4] Maastricht Univ, Cardiovasc Res Inst, NL-6200 MD Maastricht, Netherlands
关键词
polysaccharide coating; artificial surface; fibrinogen; platelets; thrombin and antithrombin;
D O I
10.1016/S0142-9612(02)00620-8
中图分类号
R318 [生物医学工程];
学科分类号
0831 ;
摘要
Heparinization of artificial surfaces has been proven to reduce the intrinsic thrombogenicity of such surfaces. The mechanism by which immobilized heparin reduces thrombogenicity is not completely understood. In the present study heparin-, alginic acid- and chondroitin-6-sulphate-coated surfaces were examined for protein adsorption, platelet adhesion and thrombin generation. The protein-binding capacity from solutions of purified proteins was significantly higher for heparin-coated surfaces when compared with alginic acid- and chondroitin sulphate-coated surfaces. Yet, when the surfaces were exposed to flowing plasma, only the heparinized surface adsorbed significant amounts of antithrombin. None of the surfaces adsorbed fibrinogen under these conditions, and as a result no platelets adhered from flowing whole blood. Our results indicate that protein adsorption and platelet adhesion from anticoagulated blood cannot be used to assess the thrombogenicity of (coated) artificial surfaces. Indeed, the thrombin generation potentials of the different surfaces varied remarkable: while non-coated surface readily produced thrombin, alginic acid- and chondroitin sulphate-coated surfaces showed a marked reduction and virtually no thrombin was generated in flowing whole blood passing by heparinized surfaces. (C) 2003 Elsevier Science Ltd. All rights reserved.
引用
收藏
页码:1917 / 1924
页数:8
相关论文
共 35 条
[1]   MECHANISM OF THE ANTICOAGULANT ACTION OF HEPARIN [J].
BJORK, I ;
LINDAHL, U .
MOLECULAR AND CELLULAR BIOCHEMISTRY, 1982, 48 (03) :161-182
[2]  
Blezer R, 1997, J BIOMED MATER RES, V37, P108, DOI 10.1002/(SICI)1097-4636(199710)37:1<108::AID-JBM13>3.0.CO
[3]  
2-C
[4]   Heparin coating of the stent graft - effects on platelets, coagulation and complement activation [J].
Christensen, K ;
Larsson, R ;
Emanuelsson, H ;
Elgue, G ;
Larsson, A .
BIOMATERIALS, 2001, 22 (04) :349-355
[5]  
CROWTHER MA, 2001, HEMOSTASIS THROMBOSI, P1497
[6]  
CUYPERS PA, 1983, J BIOL CHEM, V258, P2426
[7]  
Hanson S.R., 1996, BIOMATER SCI-UK, P193
[8]   PLATELETS INTERACT WITH FIBRIN ONLY AFTER ACTIVATION [J].
HANTGAN, RR ;
TAYLOR, RG ;
LEWIS, JC .
BLOOD, 1985, 65 (06) :1299-1311
[9]  
Heemskerk JWM, 2002, THROMB HAEMOSTASIS, V88, P186
[10]   Collagen but not fibrinogen surfaces induce bleb formation, exposure of phosphatidylserine, and procoagulant activity of adherent platelets: Evidence for regulation by protein tyrosine kinase-dependent Ca2+ responses [J].
Heemskerk, JWM ;
Vuist, WMJ ;
Feijge, MAH ;
Reutelingsperger, CPM ;
Lindhout, T .
BLOOD, 1997, 90 (07) :2615-2625