Lack of influence of the COX inhibitors metamizol and diclofenac on platelet GPIIb/IIIa and P-selectin expression in vitro.

Dirk Scheinichen,Rodin Osorio,Siegfried Piepenbrock,Karsten Jaeger,Björn Jüttner,Holger-Andreas Elsner,Werner Gröschel

doi:10.1186/1471-2253-4-4

Dirk Scheinichen, Rodin Osorio + Show 5 more

Open Access

https://doi.org/10.1186/1471-2253-4-4

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Journal: BMC anesthesiology	Publication Date: Apr 23, 2004
Citations: 32	License type: cc-by

Affiliation: Hannover Medical School

Abstract

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.

Highlights

The effect of non-steroidal anti-inflammatory drugs (NSAIDs) for reduced platelet aggregation and thromboxane A2 synthesis has been well documented
Conclusions: 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
To further study the effect of the NSAIDs diclofenac and metamizol on platelet function, we have investigated the surface expression of GPIIb/IIIa and Pselectin as well as the formation of platelet-monocyte/ granulocyte complexes, using a flow cytometric technique

Summary

Introduction

The effect of non-steroidal anti-inflammatory drugs (NSAIDs) for reduced platelet aggregation and thromboxane A2 synthesis has been well documented. Aim of this study was to examine the influence of the COX1 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. The activation of platelets is associated with a change in the expression of surface antigens, of which P-selectin and the fibrinogen receptor complex GIIb/IIIa are of special importance. P-selectin is rapidly transported to the cell surface by fusion of the α-granule membrane with the plasma membrane. P-selectin is involved in the adhesion of activated platelets to endothelium, monocytes and granulocytes. Findings from previous studies have shown that platelet activation is a potent stimulus for platelet-neutrophil complex formation and neutrophil function [1,2]

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