• Dirk Scheinichen, Holger-Andreas Elsner, Rodin Osorio, Björn Jüttner, Werner Gröschel, Karsten Jaeger, and Siegfried Piepenbrock.
• Department of Anesthesiology, Hannover Medical School, Carl-Neuberg-Str, 1, 30625 Hannover, Germany. scheinichen.dirk@mh-hannover.de
• BMC Anesthesiol. 2004 Apr 23; 4 (1): 4.

BackgroundThe effect of non-steroidal anti-inflammatory drugs (NSAIDs) for reduced platelet aggregation and thromboxane A2 synthesis has been well documented. However, the influence on platelet function is not fully explained. Aim of this study was to examine the influence of the COX-1 inhibiting NSAIDs, diclofenac and metamizol on platelet activation and leukocyte-platelet complexes, in vitro. Surface expression of GPIIb/IIIa and P-selectin on platelets, and the percentage of platelet-leukocyte complexes were investigated. MethodsWhole blood was incubated with three different concentrations of diclofenac and metamizol for 5 and 30 minutes, followed by activation with TRAP-6 and ADP. Rates of GPIIb/IIIa and P-selectin expression, and the percentage of platelet-leukocyte complexes were analyzed by a flow-cytometric assay. ResultsThere were no significant differences in the expression of GPIIb/IIIa and P-selectin, and in the formation of platelet-leukocyte complexes after activation with ADP and TRAP-6, regarding both the time of incubation and the concentrations of diclofenac and metamizol. ConclusionsAccordingly, the inhibitory effect of diclofenac and metamizol on platelet aggregation is not related to a reduced surface expression of P-selectin and GPIIb/IIIa on platelets.

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