title: Hemostatic function of apheresis platelets stored at 4°C and 22°C.
abstract: BACKGROUND
  Platelet refrigeration decreases the risk of bacterial contamination and may preserve function better than standard-of-care room temperature (RT) storage. Benefits could include lower transfusion-related complications, decreased costs, improved hemostasis in acutely bleeding patients, and extended shelf life. In this study, we compared the effects of 22°C and 4°C storage on the functional and activation status of apheresis platelets.
  
  
  METHODS
  Apheresis platelets (n = 5 per group) were stored for 5 days at 22°C with agitation (RT) versus at 4°C with agitation (4°C + AG) and without (4°C). Measurements included platelet counts, mean platelet volume, blood gas analytes, aggregation response, thromboelastography, thromboxane B2 and soluble CD40 ligand release, activation markers, and microparticle formation.
  
  
  RESULTS
  Sample pH levels were within acceptable limits for storage products (pH 6.2-7.4). Platelet glucose metabolism (P < 0.05), aggregation response (adenosine diphosphate: RT 0; 4°C + AG 5.0 ± 0.8; 4°C 5.6 ± 0.9; P < 0.05), and clot strength (maximum amplitude: RT 58 ± 2; 4°C + AG 63 ± 2; 4°C 67 ± 2; P < 0.05) were better preserved at 4°C compared with RT storage. Refrigerated samples were more activated compared with RT (P < 0.05), although thromboxane B2 (P < 0.05) and soluble CD40 ligand release (P < 0.05) were higher at RT. Agitation did not improve the quality of 4°C-stored samples.
  
  
  CONCLUSIONS
  Apheresis platelets stored at 4°C maintain more viable metabolic characteristics, are hemostatically more effective, and release fewer proinflammatory mediators than apheresis platelets stored at RT over 5 days. Given the superior bacteriologic safety of refrigerated products, these data suggest that cold-stored platelets may improve outcomes for acutely bleeding patients.
authors.affiliation: *Department of Biomedical Engineering, The University of Texas at San Antonio, San Antonio, Texas; and †US Army Institute of Surgical Research, Fort Sam Houston, Texas.
authors.forename: Kristin M
authors.initials: KM
authors.lastname: Reddoch
authors.forename: Heather F
authors.initials: HF
authors.lastname: Pidcoke
authors.forename: Robbie K
authors.initials: RK
authors.lastname: Montgomery
authors.forename: Chriselda G
authors.initials: CG
authors.lastname: Fedyk
authors.forename: James K
authors.initials: JK
authors.lastname: Aden
authors.forename: Anand K
authors.initials: AK
authors.lastname: Ramasubramanian
authors.forename: Andrew P
authors.initials: AP
authors.lastname: Cap
mesh_terms: D001424:Bacterial Infections / Q000517:prevention & control; D001781:Blood Component Removal / Q000379:methods*; D001792:Blood Platelets / Q000502:physiology*; D001793:Blood Preservation / Q000379:methods*; D023201:CD40 Ligand / Q000378:metabolism; D006489:Hemostatic Techniques; D006801:Humans; D010974:Platelet Aggregation; D013696:Temperature; D013916:Thrombelastography / Q000379:methods; D013929:Thromboxane B2 / Q000378:metabolism; D013997:Time Factors
chemical_list: D023201:CD40 Ligand; D013929:Thromboxane B2