Prolonged maintenance of 2,3‐diphosphoglycerate acid and adenosine triphosphate in red blood cells during storage

Korte, Dirk de; Kleine, Mya; Korsten, Herbert; Verhoeven, Arthur J.

doi:10.1111/j.1537-2995.2008.01689.x

Cited by 71 publications

(122 citation statements)

References 28 publications

(28 reference statements)

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“…This faster increase in stiffness during the last 3 weeks of storage can be attributed to the timing of ATP degradation. The ATP level has been shown to remain largely unchanged during the first 3 weeks of storage, but starts to drastically decrease in Week 4 41,42 , as shown in Figure 6. It is thus likely that the increase in stiffness of the stored RBCs in Week 4-Week 6 is mostly caused by the depletion of ATP.…”

Section: Rbc Effective Stiffness Increases During Storagementioning

confidence: 89%

“…There also are some technical issue that deserves more investigation. To better understand the effect of biochemical degradation on the changes in RBC stiffness, performing biochemical measurements on single RBCs and stiffness measurements on the same RBCs, different from existing studies on RBC populations [40][41][42] , would permit a more precise correlation.…”

Section: Rbc Effective Stiffness Increases During Storagementioning

confidence: 99%

“…Another protein, protein 4.1, also plays a key role in regulating membrane stiffness by interacting with spectrin and glycophorin, and their interactions are modulated by phosphorylation, a process that involves the addition of a phosphate to an organic compound by consuming ATP 39 . The structure and the interactions between these proteins change during RBC storage due to the degradation of several biochemical parameters, such as SNO and ATP [40][41][42] . The degradation of these biochemical parameters over the RBC storage process has been widely reported, and the depletion of SNO and ATP has been speculated to play important roles in regulating RBCs' mechanical properties 39,[43][44][45] .…”

Section: Rbc Effective Stiffness Increases During Storagementioning

confidence: 99%

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Stiffness increase of red blood cells during storage

Zheng

Wang

et al. 2018

Microsyst Nanoeng

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In transfusion medicine, the deformability of stored red blood cells (RBCs) changes during storage in blood banks. Compromised RBC deformability can reduce the transfusion efficiency or intensify transfusion complications, such as sepsis. This paper reports the microfluidic mechanical measurement of stored RBCs under the physiological deformation mode (that is, folding). Instead of using phenomenological metrics of deformation or elongation indices (DI or EI), the effective stiffness of RBCs, a flow velocityindependent parameter, is defined and used for the first time to evaluate the mechanical degradation of RBCs during storage. Fresh RBCs and RBCs stored up to 6 weeks (42 days) in the blood bank were measured, revealing that the effective stiffness of RBCs increases over the storage process. RBCs stored for 1 week started to show significantly higher stiffness than fresh RBCs, and stored RBC stiffness degraded faster during the last 3 weeks than during the first 3 weeks. Furthermore, the results indicate that the time points of the effective stiffness increase coincide well with the degradation patterns of S-nitrosothiols (SNO) and adenosine triphosphate (ATP) in RBC storage lesions.

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Section: Rbc Effective Stiffness Increases During Storagementioning

confidence: 89%

Section: Rbc Effective Stiffness Increases During Storagementioning

confidence: 99%

Section: Rbc Effective Stiffness Increases During Storagementioning

confidence: 99%

See 1 more Smart Citation

Stiffness increase of red blood cells during storage

Zheng

Wang

et al. 2018

Microsyst Nanoeng

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“…DPG is typically gone by the 10th day of red blood cell storage, whereas ATP concentrations initially increase or are stable during the first 2 to 4 weeks of storage with generally declining concentrations thereafter. New experimental solutions may be able to extend high concentrations of ATP longer [17].…”

Section: Standards For Red Blood Cell Storage: Recovery Survival Andmentioning

confidence: 99%

Current issues relating to the transfusion of stored red blood cells

Zimrin¹,

2009

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The development of blood storage systems allowed donation and transfusion to be separated in time and space. This separation has permitted the regionalization of donor services with subsequent economies of scale and improvements in the quality and availability of blood products. However, the availability of storage raises the question of how long blood products can and should be stored and how long they are safe and effective. The efficacy of red blood cells was originally measured as the increment in haematocrit and safety began with typing and the effort to reduce the risk of bacterial contamination. Appreciation of a growing list of storage lesions of red blood cells has developed with our increasing understanding of red blood cell physiology and our experience with red blood cell transfusion. However, other than frank haemolysis, rare episodes of bacterial contamination and overgrowth, the reduction of oxygen-carrying capacity associated with the failure of some transfused cells to circulate, and the toxicity of lysophospholipids released from membrane breakdown, storage-induced lesions have not had obvious correlations with safety or efficacy. The safety of red blood cell storage has also been approached in retrospective epidemiologic studies of transfused patients, but the results are frequently biased by the fact that sicker patients are transfused more often and blood banks do not issue blood products in a random order. Several large prospective studies of the safety of stored red blood cells are planned.

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“…RBC were diluted to a hematocrit (Ht) of 50% in PBS supplemented with 5.5 mM glucose. RBC were incubated at 37 C, and samples were taken for ATP measurements at the start of the incubation, and after 24 and 48 h. ATP was measured as described [14].…”

Section: Methodsmentioning

confidence: 99%

Partial pyruvate kinase deficiency aggravates the phenotypic expression of band 3 deficiency in a family with hereditary spherocytosis

et al. 2014

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In a family with mild dominant spherocytosis, affected members showed partial band 3 deficiency. The index patient showed more severe clinical symptoms than his relatives, and his red blood cells displayed concomitant low pyruvate kinase activity. We investigated the contribution of partial PK deficiency to the phenotypic expression of mutant band 3 in this family. Pyruvate kinase deficiency and band 3 deficiency were characterized by DNA analysis. Results of red cell osmotic fragility testing, the results of cell deformability obtained by the Automated Rheoscope and Cell Analyzer and the results obtained by Osmotic Gradient Ektacytometry, which is a combination of these tests, were related to the red cell ATP content. Spherocytosis in this family was due to a novel heterozygous mutation in SLC4A1, the gene for band 3. Reduced PK activity of the index patient was attributed to a novel mutation in PKLR inherited from his mother, who was without clinical symptoms. Partial PK deficiency was associated with decreased red cell ATP content and markedly increased osmotic fragility. This suggests an aggravating effect of low ATP levels on the phenotypic expression of band 3 deficiency.Am. J. Hematol. 90:E35-E39,

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Prolonged maintenance of 2,3‐diphosphoglycerate acid and adenosine triphosphate in red blood cells during storage

Abstract: Resuspension of RBCs in our alkaline medium PAGGG-M resulted in a RBC unit of high quality during storage for up to at least 35 days, with 2,3-DPG levels of higher than 10 mumol per g Hb, hemolysis of less than 0.2 percent, and ATP levels of higher than 5 mumol per g Hb.

Cited by 71 publications

References 28 publications

Stiffness increase of red blood cells during storage

Stiffness increase of red blood cells during storage

Current issues relating to the transfusion of stored red blood cells

Partial pyruvate kinase deficiency aggravates the phenotypic expression of band 3 deficiency in a family with hereditary spherocytosis

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