title: Antithrombin significantly influences platelet adhesion onto immobilized fibrinogen in an in-vitro system simulating low flow.
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).
  
  
  CONCLUSIONS
  It appears that antithrombin in a low flow system suppresses platelet adhesion onto immobilized fibrinogen independently from its antithrombin activity. A supraphysiological substitution of blood with antithrombin significantly reduces platelet adhesion rate. This inhibitory effect might be of clinical relevance.
authors.affiliation: Department of Hemostasis and Transfusion Medicine, Heinrich Heine University Medical Center Duesseldorf, Germany. Loncar@med.uni-duesseldorf.de
authors.forename: Robert
authors.initials: R
authors.lastname: Loncar
authors.forename: Uwe
authors.initials: U
authors.lastname: Kalina
authors.forename: Volker
authors.initials: V
authors.lastname: Stoldt
authors.forename: Volker
authors.initials: V
authors.lastname: Thomas
authors.forename: Rüdiger E
authors.initials: RE
authors.lastname: Scharf
authors.forename: Aleksandar
authors.initials: A
authors.lastname: Vodovnik