CC BY 4.0 · TH Open 2020; 04(03): e163-e172
DOI: 10.1055/s-0040-1714254
Original Article

The Impact of Cold Storage on Adenosine Diphosphate-Mediated Platelet Responsiveness

1   Institute of Clinical Transfusion Medicine and Haemotherapy, University of Wuerzburg, Germany
,
Philipp Klingler
1   Institute of Clinical Transfusion Medicine and Haemotherapy, University of Wuerzburg, Germany
,
Marius Niklaus
1   Institute of Clinical Transfusion Medicine and Haemotherapy, University of Wuerzburg, Germany
,
Katja Weber
1   Institute of Clinical Transfusion Medicine and Haemotherapy, University of Wuerzburg, Germany
,
Angela Koessler
1   Institute of Clinical Transfusion Medicine and Haemotherapy, University of Wuerzburg, Germany
,
Markus Boeck
1   Institute of Clinical Transfusion Medicine and Haemotherapy, University of Wuerzburg, Germany
,
Anna Kobsar
1   Institute of Clinical Transfusion Medicine and Haemotherapy, University of Wuerzburg, Germany
› Author Affiliations
Funding This publication was supported by the Open Access Publication Fund of the University of Wuerzburg. The study was funded by the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation), project number: KO 5256/3-1 (J.K.) and KO 5294/2-1 (A.Kob.).

Abstract

Introduction Cold storage of platelets is considered to contribute to lower risk of bacterial growth and to more efficient hemostatic capacity. For the optimization of storage strategies, it is required to further elucidate the influence of refrigeration on platelet integrity. This study focused on adenosine diphosphate (ADP)-related platelet responsiveness.

Materials and Methods Platelets were prepared from apheresis-derived platelet concentrates or from peripheral whole blood, stored either at room temperature or at 4°C. ADP-induced aggregation was tested with light transmission. Activation markers, purinergic receptor expression, and P2Y12 receptor function were determined by flow cytometry. P2Y1 and P2X1 function was assessed by fluorescence assays, cyclic nucleotide concentrations by immunoassays, and vasodilator-stimulated phosphoprotein (VASP)-phosphorylation levels by Western blot analysis.

Results In contrast to room temperature, ADP-induced aggregation was maintained under cold storage for 6 days, associated with elevated activation markers like fibrinogen binding or CD62P expression. Purinergic receptor expression was not essentially different, whereas P2Y1 function deteriorated rapidly at cold storage, but not P2Y12 activity. Inhibitory pathways of cold-stored platelets were characterized by reduced responses to nitric oxide and prostaglandin E1. Refrigeration of citrated whole blood also led to the attenuation of induced inhibition of platelet aggregation, detectable within 24 hours.

Conclusion ADP responsiveness is preserved under cold storage for 6 days due to stable P2Y12 activity and concomitant disintegration of inhibitory pathways enabling a higher reactivity of stored platelets. The ideal storage time at cold temperature for the highest hemostatic effect of platelets should be evaluated in further studies.



Publication History

Received: 27 March 2020

Accepted: 09 June 2020

Article published online:
13 August 2020

© 2020. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution License, permitting unrestricted use, distribution, and reproduction so long as the original work is properly cited. (https://creativecommons.org/licenses/by/4.0/).

Georg Thieme Verlag KG
Stuttgart · New York

 
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