Thromb Haemost 1995; 73(05): 850-856
DOI: 10.1055/s-0038-1653880
Original Articles
Platelets
Schattauer GmbH Stuttgart

Platelet Accumulation on Fibrin-coated Polyethylene: Role of Platelet Activation and Factor XIII

F D Rubens
1   The Department of Pathology, McMaster University, Canada
,
D W Perry
1   The Department of Pathology, McMaster University, Canada
,
M W C Hatton
1   The Department of Pathology, McMaster University, Canada
,
P D Bishop
2   Zymogenetics Inc., Seattle, Washington, U.S.A.
,
M A Packham
3   Department of Biochemistry, University of Toronto, Ontario, Canada
,
R L Kinlough-Rathbone
1   The Department of Pathology, McMaster University, Canada
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Publikationsverlauf

Received 01. August 1994

Accepted after resubmission 24. Januar 1995

Publikationsdatum:
09. Juli 2018 (online)

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Summary

Platelet accumulation on small- and medium-calibre vascular grafts plays a significant role in graft occlusion. We examined platelet accumulation on the surface of fibrin-coated polyethylene tubing (internal diameter 0.17 cm) during 10 min of flow (l0ml/min) at high wall shear rate (764 s-1). Washed platelets labelled with 51Cr were resuspended in Tyrode solution containing albumin, apyrase and red blood cells (hematocrit 40%). When the thrombin that was used to form the fibrin-coated surface was inactivated with FPRCH2C1 before perfusion of the tubes with the platelet:red blood cell suspension, the accumulation of platelets was 59,840 ± 27,960 platelets per mm2, whereas accumulation on fibrin with residual active thrombin was 316,750 ± 32,560 platelets per mm2 (n = 4). When the fibrin on the surface was cross-linked by including recombinant factor XIII (rFXIII) in the fibrinogen solution used to prepare the fibrin-coated surface, platelet accumulation, after thrombin neutralization, was reduced by the cross-linking from 46,974 ± 9702 to 36,818 ± 7964 platelets per mm2 (n = 12, p <0.01). Platelet accumulation on tubes coated with D-dimer was ten times less than on tubes coated with D-domain; this finding also supports the observation that cross-linking of fibrin with the formation of γ-γ dimers reduces platelet accumulation on the fibrin-coated surface. Thrombin-activated platelets themselves were shown to cross-link fibrin when they had adhered to it during perfusion, or in a static system in which thrombin was used to form clots from FXIII-free fibrinogen in the presence of platelets. Thus, cross-linking of fibrin by FXIII in plasma or from platelets probably decreases the reactivity of the fibrin-containing thrombi to platelets by altering the lysine residue at or near the platelet-binding site of each of the γ-chains of the fibrinogen which was converted into the fibrin of these thrombi.