Storage of platelets at 4°C in platelet additive solutions prevents aggregate formation and preserves platelet functional responses
-
- Todd M. Getz
- US Army Institute of Surgical Research Fort Sam Houston, San Antonio Texas
-
- Robbie K. Montgomery
- US Army Institute of Surgical Research Fort Sam Houston, San Antonio Texas
-
- James A. Bynum
- US Army Institute of Surgical Research Fort Sam Houston, San Antonio Texas
-
- James K. Aden
- US Army Institute of Surgical Research Fort Sam Houston, San Antonio Texas
-
- Heather F. Pidcoke
- US Army Institute of Surgical Research Fort Sam Houston, San Antonio Texas
-
- Andrew P. Cap
- US Army Institute of Surgical Research Fort Sam Houston, San Antonio Texas
説明
<jats:sec><jats:title>BACKGROUND</jats:title><jats:p>Platelet (PLT) storage has been limited to 5 days at room temperature due to metabolic decline and risk for bacterial contamination. Refrigeration preserves PLT metabolism and function as well as limits bacterial growth; however, cold storage of PLTs also leads to aggregate formation. We hypothesized that storage of PLT concentrates at 4°C leads to glycoprotein (GP)IIb‐IIIa activation and thus aggregate formation through fibrinogen binding and that this could be prevented by storing PLTs in PLT additive solution (PAS) without compromising PLT function.</jats:p></jats:sec><jats:sec><jats:title>STUDY DESIGN AND METHODS</jats:title><jats:p>Apheresis PLTs in plasma (AP) or apheresis PLTs in PAS were stored at 22 or 4°C for up to 15 days. Measurements include PLT counts, blood gases, aggregation response, flow cytometry analysis of integrin levels, activation markers, and microparticle formation.</jats:p></jats:sec><jats:sec><jats:title>RESULTS</jats:title><jats:p>Storage of AP 4°C led to a gradual decline in PLT count and an increase in aggregate formation that was mediated by intracellular calcium leak and fibrinogen receptor activation. Storage of PAS at 4°C prevented aggregate formation due to dilution of plasma fibrinogen. PAS stored at 4°C maintained aggregation responses to multiple agonists better than 22°C controls.</jats:p></jats:sec><jats:sec><jats:title>CONCLUSION</jats:title><jats:p>Storage of AP at 4°C leads to low level GPIIb‐IIIa activation and results in aggregate formation over time. Separating the PLTs from the plasma component and storing them in PAS at 4°C resolves aggregate formation and preserves the metabolic and functional responses of these stored PLTs.</jats:p></jats:sec>
収録刊行物
-
- Transfusion
-
Transfusion 56 (6), 1320-1328, 2016-02-08
Wiley