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Research Article Free access | 10.1172/JCI106504

Platelet storage at 22°C; metabolic, morphologic, and functional studies

Scott Murphy and Frank H. Gardner

1Research Hematology Laboratory, Presbyterian-University of Pennsylvania Medical Center and The Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104

Find articles by Murphy, S. in: PubMed | Google Scholar

1Research Hematology Laboratory, Presbyterian-University of Pennsylvania Medical Center and The Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104

Find articles by Gardner, F. in: PubMed | Google Scholar

Published February 1, 1971 - More info

Published in Volume 50, Issue 2 on February 1, 1971
J Clin Invest. 1971;50(2):370–377. https://doi.org/10.1172/JCI106504.
© 1971 The American Society for Clinical Investigation
Published February 1, 1971 - Version history
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Abstract

Platelets stored at 22°C for transfusion purpose have been examined with metabolic, morphologic, and functional studies. Evaluations were made of platelet-rich plasma (PRP) stored for 3-4 days and platelet concentrates (PC) stored for 24 hr. During these periods, lactate accumulated continuously without significant change in platelet count, pH, or plasma glucose. Platelet glycogen fell dramatically both chemically and by electron microscopy, but adenosine triphosphate (ATP), adenosine diphosphate (ADP), and intracellular potassium did not change. After storage, the cell's capacity for glucose utilization through glycolysis, the hexose monophosphate shunt, and the tricarboxylic acid cycle appeared to be intact. Although platelet volume during storage did not change, disc to sphere transformation was observed by phase microscopy. Platelet aggregration with ADP was reduced even after 1 day of storage. After transfusion of stored platelets to thrombocytopenic recipients, recovery of platelet glycogen and capacity for aggregation occurred within 24 hr. In summary, the platelet remains surprisingly intact during the intervals studied; those defects which do develop are reversible in the circulation of a thrombocytopenic recipient if viability has been maintained. A “storage lesion” responsible for loss of viability has not been defined.

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