Antithrombin significantly influences platelet adhesion onto immobilized fibrinogen in an in-vitro system simulating low

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BioMed Central

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Original basic research

Antithrombin significantly influences platelet adhesion onto immobilized fibrinogen in an in-vitro system simulating low flow Robert Loncar*1, Uwe Kalina2, Volker Stoldt1, Volker Thomas1, Rüdiger E Scharf1 and Aleksandar Vodovnik3 Address: 1Department of Hemostasis and Transfusion Medicine, Heinrich Heine University Medical Center Duesseldorf, Germany, 2Research ZLB Behring, Emil von Behring Strasse 76, 35041 Marburg, Germany and 3Department of Histopathology, The Calderdale Royal Hospital, HX3 0PA Halifax, UK Email: Robert Loncar* - [email protected]; Uwe Kalina - [email protected]; Volker Stoldt - [email protected]; Volker Thomas - [email protected]; Rüdiger E Scharf - [email protected]; Aleksandar Vodovnik - [email protected] * Corresponding author

Published: 13 October 2006 Thrombosis Journal 2006, 4:19

doi:10.1186/1477-9560-4-19

Received: 04 May 2006 Accepted: 13 October 2006

This article is available from: http://www.thrombosisjournal.com/content/4/1/19 © 2006 Loncar et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract Background: Adhesion of platelets onto immobilized fibrinogen is of importance in initiation and development of thrombosis. According to a recent increase in evidence of a multiple biological property of antithrombin, we evaluated the influence of antithrombin on platelet adhesion onto immobilized fibrinogen using an in-vitro flow system. Methods: Platelets in anticoagulated whole blood (29 healthy blood donors) were labelled with fluorescence dye and perfused through a rectangular flow chamber (shear rates of 13 s-1 to 1500 s-1). Platelet adhesion onto fibrinogen-coated slips was assessed using a fluorescence laser-scan microscope and compared to the plasma antithrombin activity. Additionally the effect of supraphysiological AT supplementation on platelets adhesion rate was evaluated. Results: Within a first minute of perfusion, an inverse correlation between platelet adhesion and plasma antithrombin were observed at 13 s-1 and 50 s-1 (r = -0.48 and r = -0.7, p < 0.05, respectively). Significant differences in platelet adhesion related to low (92 ± 3.3%) and high (117 ± 4.1%) antithrombin activity (1786 ± 516 U vs. 823 ± 331 U, p < 0.05) at low flow rate (13 s-1, within first minute) have been found. An in-vitro supplementation of whole blood with antithrombin increased the antithrombin activity up to 280% and platelet adhesion rate reached about 65% related to the adhesion rate in a non-supplemented blood (1.25 ± 0.17 vs. 1.95 ± 0.4 p = 0.008, respectively). Conclusion: It appears that antithrombin in a low flow system suppresses platelet adhesion onto immobilized fibrinogen independently from its a