Erschienen in:
01.07.2003 | Experimental
Effect of propofol on adhesion of activated platelets to leukocytes in human whole blood
verfasst von:
Lothar de Rossi, Martina Wessiepe, Wolfgang Buhre, Ralf Kuhlen, Gabriele Hutschenreuter, Rolf Rossaint
Erschienen in:
Intensive Care Medicine
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Ausgabe 7/2003
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Abstract
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 µg/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 µg/ml concentration of propofol did not alter binding of platelets to leukocytes, expression of P-selectin, GPIb and fibrinogen binding to platelets. The 40 µg/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 µg/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 µg/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.