High-yield Platelet units revealed immediate pH decline and delayed mitochondrial dysfunction during storage in 100% plasma as compared with storage in SSP+


Dr Per Sandgren, Departments of Clinical Immunology and Transfusion Medicine, Karolinska University Hospital and Karolinska Institutet, 141 86 Stockholm, Sweden
E-mail: per.sandgren@karolinska.se


Background and Objectives  Initial elevated and prolonged high carbon dioxide levels related to mitochondrial dysfunction are recently being suggested as a contributing factor to rapid pH decline in platelet (PLT) units. The use of different storage environments may influence this phenomenon. This study has two objectives (i) to investigate the relationship of mitochondrial function and apoptotic events with different storage environments capability of pH control and (ii) to examine the cause and relationship between pH decline in PLT units, carbon dioxide levels and mitochondrial function.

Materials and Methods  Platelet units were prepared for storage in (A) 70% SSP+, 300–400 × 109/unit, (B) 70% SSP+, 550–600 × 109/unit, (C) 100% plasma, 550–600 × 109/unit, and (D) additional 100% plasma, >600 × 109/unit. In vitro variables including mitochondrial function (JC-1), reactive oxygen species (ROS) and caspase 3 activity were analysed on days 2, 5 and 7.

Results  Glucose/lactate was higher, pH, ATP, Hypotonic shock response (HSR) and extent of shape change (ESC) decreased (P < 0·001 on day 7), CD62P (P < 0·001 on day 7) increased, the JC-1-positive PLTs were lower (P < 0·001 on day 7), and ROS was higher (P < 0·001 days 2–7) in the plasma (C) units as compared with the SSP+ (A) and (B) units. All plasma (D) units showed rapid pH and pCO2 decline from day 2 but by means of >80% maintenance of mitochondrial function until day 7.

Conclusions  The use of SSP+ instead of plasma may reduce the risk of triggering pro-apoptotic events in high-yield PLT units. A rapid decline in pH in PLT units cannot be explained with initial elevated and prolonged high carbon dioxide levels and mitochondrial dysfunction.