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Updated: Jul 13, 2026

Ex Vivo Perfusion of the Rodent Placenta
Published on: May 30, 2019
Evaluation of nonleukoreduced red blood cell transfusion units collected at delivery from the placenta
Line Widing1, Anne Grete Bechensteen, Mohammad Reza Mirlashari
1Departments of Pediatrics and Immunology & Transfusion Medicine, Ullevål University Hospital, University of Oslo, Kirkeveien 166, N-0407 Oslo, Norway.
Background:
The objective of this study was to evaluate the suitability of cord blood (CB) as a source of red blood cells (RBCs) for autologous transfusion.
Study Design And Methods:
CB was collected in 150-mL storage containers with citrate phosphate dextrose (CPD) as anticoagulant and stored in either saline, adenine, glucose, and mannitol (SAG-M; n = 18) or phosphate, adenine, glucose, guanosine, saline, and mannitol (PAGGS-M; n = 18) for 35 days at 4 degrees C. Hematologic status and hemolysis were studied. The lipopolysaccharide (LPS)-induced production of tumor necrosis factor (TNF)-alpha and transforming growth factor (TGF)-beta1 from CB monocytes was analyzed after incubation with addition of weekly sampled supernatants from the CB RBC units. Five additional units (PAGGS-M) were leukoreduced and thereafter analyzed as indicated above.
Results:
Hemolysis increased significantly over time, in SAG-M more than in PAGGS-M. During storage in both media, the number of white blood cells (WBCs) decreased, and the LPS-induced production of TNF-alpha and TGF-beta1 decreased and increased, respectively. There were no significant changes in the LPS-induced production of TNF-alpha and TGF-beta1 in the leukoreduced CB RBC units.
Conclusion:
Hemolysis in CB RBC units increased significantly over time, and PAGGS-M appears to be superior to SAG-M as a preservation solution for CB RBC. The changes in LPS-induced TNF-alpha and TGF-beta1 production over time were probably caused by substances released from apoptotic and/or necrotic WBCs. Further studies are needed to identify both which substances are responsible for the changes in LPS-induced cytokine release and the clinical significance hereof.
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