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Updated: Aug 7, 2026

Dynamic Multiparameter Platelet Function Assessment Using a Capacitive Biosensor
Published on: May 2, 2025
Effect of propofol on adhesion of activated platelets to leukocytes in human whole blood
Lothar de Rossi1, Martina Wessiepe, Wolfgang Buhre
1Department of Anaesthesiology, University Hospital, Rheinisch-Westfälische Technische Hochschule Aachen, Pauwelsstr. 30, 52074, Aachen, Germany. L.derossi@gmx.de
Objective:
To investigate the effect of propofol and its solvent Intralipid on the adhesion of activated platelets to leukocytes in vitro.
Design And Setting:
Prospective study in an experimental laboratory.
Participants:
Sixteen healthy volunteers.
Interventions:
Whole blood was incubated for 60 min with propofol (4, 40 micro g/ml), an equal volume of Intralipid 10% or phosphate-buffered saline (PBS). After stimulation with adenosine-5-diphosphate (ADP) platelet-leukocyte adhesion and platelet surface expression of P-selectin, GPIb and fibrinogen-binding to platelets were evaluated by flow cytometry.
Measurements And Results:
The 4 micro g/ml concentration of propofol did not alter binding of platelets to leukocytes, expression of P-selectin, GPIb and fibrinogen binding to platelets. The 40 micro g/ml concentration of propofol reduced spontaneous and ADP-induced formation of platelet-neutrophil conjugates compared with PBS and the equal volume of Intralipid. In addition, binding of ADP-activated platelets to monocytes were also inhibited by 40 micro g/ml propofol. Following incubation with propofol, platelets showed reduced binding of fibrinogen in the unstimulated and ADP-stimulated blood samples as well as a lower percentage of platelets with bound fibrinogen. Effects dependent on the solvent Intralipid were enhanced adhesion of platelets to monocytes in comparison with propofol (40 micro g/ml) and PBS.
Conclusion:
In clinically used concentrations, propofol does not alter the adhesion of platelets to leukocytes in vitro. At ten-fold anesthetic concentration propofol reduced the formation of platelet-neutrophil and platelet-monocyte conjugates. We suggest that this effect is due to an inhibition of fibrinogen-binding to platelets by propofol. These effects were all independent of the propofol carrier Intralipid.
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