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ANESTHETIC PHARMACOLOGY

Xenon Does Not Affect Human Platelet Function In Vitro

Lothar W. de Rossi, MD^*, Nicola A. Horn, MD^*, Jan H. Baumert, MD^*, Kai Gutensohn, MD, Gabriele Hutschenreuter, MD, and Rolf Rossaint, MD^*

*Department of Anesthesiology, University Hospital, Rheinisch-Westfälische Technische Hochschule Aachen, Aachen, Germany; Department of Transfusion Medicine/Transplantation Immunology, University Hospital Eppendorf, Hamburg, Germany; and Institute of Transfusion Medicine, University Hospital, Rheinisch-Westfälische Technische Hochschule Aachen, Aachen, Germany

Address correspondence and reprint requests to Lothar W. de Rossi, MD, Department of Anesthesiology, University Hospital, Rheinisch-Westfälische Technische Hochschule Aachen, Pauwelsstr. 30, D-52074 Aachen, Germany. Address e-mail to L.derossi{at}gmx.de

We sought to determine whether xenon affects platelet glycoprotein expression and platelet-related hemostasis in vitro at a clinically relevant concentration. Human whole blood was stimulated with either adenosine diphosphate or the thrombin receptor agonist peptide (TRAP)-6 after incubation with 65% xenon. Halothane at 2 minimum alveolar anesthetic concentration was used as a positive control. Platelet function and activation were evaluated with two-color flow cytometry. The expression of the platelet glycoproteins GPIIb/IIIa, GPIb, and P selectin were detected with fluorochrome-conjugated monoclonal antibodies. In vitro measurement of platelet-related hemostasis under conditions of high shear stress was performed in citrated whole blood with a platelet function analyzer (PFA-100^®) by using collagen/epinephrine and collagen/adenosine diphosphate cartridges. Xenon did not affect basal or agonist-induced expression of platelet membrane glycoproteins, activation-dependent conformational changes of the GPIIb/IIIa receptor, expression of P selectin, or PFA closure times. In contrast, halothane reduced TRAP-6-induced activation of the GPIIb/IIIa complex. Furthermore, collagen/epinephrine-induced PFA closure time was significantly prolonged. These results demonstrate that xenon does not affect the unstimulated or agonist-induced platelet glycoprotein expression, activation of GPIIb/IIIa, or platelet-related hemostasis.

IMPLICATIONS: Halothane and sevoflurane inhibit platelet aggregation. Xenon did not affect platelet glycoprotein expression or in vitro bleeding time. Because platelet glycoprotein expression is strongly related to platelet adhesion to sites of vascular injury and platelet aggregation, we suggest that xenon does not interfere with platelet function in vitro.

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