de Rossi Lothar, Wessiepe Martina, Buhre Wolfgang, Kuhlen Ralf, Hutschenreuter Gabriele, Rossaint Rolf
Department of Anaesthesiology, University Hospital, Rheinisch-Westfälische Technische Hochschule Aachen, Pauwelsstr. 30, 52074, Aachen, Germany.
Intensive Care Med. 2003 Jul;29(7):1157-63. doi: 10.1007/s00134-003-1814-z. Epub 2003 Jun 11.
To investigate the effect of propofol and its solvent Intralipid on the adhesion of activated platelets to leukocytes in vitro.
Prospective study in an experimental laboratory.
Sixteen healthy volunteers.
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.
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.
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.
研究丙泊酚及其溶剂乳剂对体外活化血小板与白细胞黏附的影响。
实验室内的前瞻性研究。
16名健康志愿者。
全血分别与丙泊酚(4、40μg/ml)、等体积的10%乳剂或磷酸盐缓冲液(PBS)孵育60分钟。用5-二磷酸腺苷(ADP)刺激后,通过流式细胞术评估血小板与白细胞的黏附以及血小板表面P-选择素、糖蛋白Ib(GPIb)的表达和纤维蛋白原与血小板的结合。
4μg/ml浓度的丙泊酚未改变血小板与白细胞的结合、P-选择素的表达、GPIb以及纤维蛋白原与血小板的结合。与PBS和等体积的乳剂相比,40μg/ml浓度的丙泊酚减少了自发和ADP诱导的血小板-中性粒细胞结合物的形成。此外,40μg/ml丙泊酚也抑制了ADP活化血小板与单核细胞的结合。与丙泊酚孵育后,在未刺激和ADP刺激的血样中,血小板显示出纤维蛋白原结合减少,以及结合纤维蛋白原的血小板百分比降低。与丙泊酚(40μg/ml)和PBS相比,依赖于溶剂乳剂的效应是血小板与单核细胞的黏附增强。
在临床使用浓度下,丙泊酚不会改变体外血小板与白细胞的黏附。在麻醉浓度的10倍时,丙泊酚减少了血小板-中性粒细胞和血小板-单核细胞结合物的形成。我们认为这种效应是由于丙泊酚抑制了纤维蛋白原与血小板的结合。这些效应均与丙泊酚载体乳剂无关。