Influence of Storage on Red Blood Cell Rheological Properties

Berezina, Tamara L.; Zaets, Sergey B.; Morgan, Claire C.; Spillert, C. R.; Kamiyama, M.; Spolarics, Zoltán; Deitch, Edwin A.; Machiedo, George W.

doi:10.1006/jsre.2001.6306

Cited by 337 publications

(310 citation statements)

References 16 publications

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“…In addition, prolonged storage leads to accumulation of potentially harmful debris, most notably, aggregates of oxidized membrane lipids and proteins [7,34,39]. RBC membrane and lipid loss and micro particle formation are probable causes for procoagulant, proinflammatory, and thrombogenic effects post-transfusion, and their potential role in context of acute lung injury will be examined in detail later in this paper (Figure 1) [40]. Collectively, the detrimental changes in RBC morphology and the accumulation of the injurious debris commonly found in stored blood are termed "storage lesion".…”

Section: Storage Lesionmentioning

confidence: 99%

Storage of Red Blood Cells and Transfusion-Related Acute Lung Injury

Babaev

Pozzi

Hare

et al. 2014

JACCOA

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Transfusion-related acute lung injury (TRALI) is a major complication posttransfusion. A consensus definition of TRALI has been recently established to improve diagnosis but the pathogenesis of TRALI is yet to be understood. Although the antibody-mediated two-hit model of TRALI is the classical narrative, increasing evidence of the probable implications of prolonged storage of blood provides novel mechanisms towards storage lesion-the potentially injurious cellular and biochemical changes that occur in stored red blood cells. Red blood cell-derived lipids and micro vesicles may have been playing an important role in the development of TRALI. This article will provide a brief overview of the current understanding of TRALI and then discuss the implications and the potential mechanisms by which stored red blood cells may lead to TRALI. TRALI is characterized by clinical features that include, but not limited to, dyspnea, tachypnea, respiratory insufficiency, noncardiogenic bilateral pulmonary edema, decreased pulmonary compliance and acute hypoxemia (PaO 2 /FiO 2 <300 mmHg, (Table 1) [13,14]. KeywordsThe incidence of TRALI ranges from 1/5,000-1/1,323 transfusions within the general population and it is the leading cause of transfusion-related death in the United States [15]. Such large range in incidence could be attributed to the relatively unspecific diagnostics tools available for TRALI, past cases of under-diagnosis or misdiagnosis, and the elevated incidence of TRALI within vulnerable populations [14][15][16]. A recent study analyzing the incidence of TRALI in critically ill patients admitted to intensive care unit (ICU) observed that over 5% of all patients who received blood transfusion developed TRALI, which is 50-100 times greater occurrence than in the general hospital population [12,17]. Risk factors related to recipients and donorsThe risk factors of TRALI are highly diverse, among patients DefinitionDiagnostic Parameters TRALIBi-lateral infiltrates with non-cardiogenic pulmonary edema. ARDS appearance within 6hours after transfusion. Hypoxemia: PaO 2 /F i O 2 < 300 mmHg. Potential TRALI Similar to TRALI diagnosis with an additional risk-factor for lung injury/ARDS. Delayed TRALI Diagnostic parameters characteristic of TRALI within 24-72 hours after transfusion.

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Section: Storage Lesionmentioning

confidence: 99%

Storage of Red Blood Cells and Transfusion-Related Acute Lung Injury

Babaev

Pozzi

Hare

et al. 2014

JACCOA

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“…Storage-associated biomechanical changes (for example, decrease in deformability) can cause a decrease in transfusion efficacy and increase in harmful effects 5,6 . Poorly deformable RBCs result in a higher clearance by the spleen and are known to contribute to respiratory distress and systemic sepsis 7,8 . Clinical research has also identified a number of disease conditions, such as splanchnic ischemia, that develop in patients who had been transfused with older RBCs.…”

Section: Introductionmentioning

confidence: 99%

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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“…Stored RBCs contribute to NO scavenging when chemical and morphological changes in RBCs occur during blood storage, especially when RBC membrane permeability to NO increases 5-70 fold as we suggest in this work. This increase in permeability can be explained in terms of damage to the red cell cytoskeleton during blood storage [50,51]. Previous work has shown that chemical or mechanical alteration of the red cell cytoskeleton results in increased red cell NO scavenging attributed to increased permeability to NO [52].…”

Section: Discussionmentioning

confidence: 99%

“…These values overlap normal clinical reference ranges for RBC MCHC (19-22 mM) and MCV (80-99 mm 3 ). In addition, it has been shown that significant changes in the RBC membrane occur during blood storage and storage leads to cytoskeletal damage [21,50,51]. Disruption of cytoskeleton results in increased NO scavenging associated with increased NO permeability [52].…”

Section: Examined Effects Of Rbc Mchc MCV and Permeabilitymentioning

confidence: 99%

Mechanism of Faster NO Scavenging by Older Stored Red Blood Cells

Liu

Janes

et al. 2013

Free Radical Biology and Medicine

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a b s t r a c tThe blood storage lesion involves morphological and biochemical changes of red blood cells (RBCs) that occur during storage. These include conversion of the biconcave disc morphology to a spherical one, decreased mean corpuscular hemoglobin concentration, varied mean corpuscular volume, reduced integrity of the erythrocyte membrane with formation of microparticles, and increased cell-free hemoglobin. We studied the extent that older stored red blood cells scavenge nitric oxide (NO) faster than fresher stored red blood cells. Using electron paramagnetic resonance spectroscopy and stoppedflow absorption spectroscopy to measure the rate of NO uptake and reaction with hemoglobin in red cells, we found that older stored red blood cells scavenge NO about 1.8 times faster than fresher ones. Based on these experimental data, we simulated NO scavenging by fresher or older stored red blood cells with a biconcave or spherical geometry, respectively, in order to explore the mechanism of NO scavenging related to changes that occur during blood storage. We found that red blood cells with a spherical geometry scavenges NO about 2 times slower than ones with a biconcave geometry, and a smaller RBC hemoglobin concentration or volume increases NO scavenging by red blood cells. Our simulations demonstrate that even the most extreme possible changes in mean corpuscular hemoglobin concentration and mean corpuscular volume that favor increased NO scavenging are insufficient to account for what is observed experimentally. Therefore, RBC membrane permeability must increase during storage and we find that the permeability is likely to increase between 5 and 70 fold. Simulations using a two-dimensional blood vessel show that even a 5-fold increase in membrane permeability to NO can reduce NO bioavailability at the smooth muscle. Background: Transfusion of older stored blood may be harmful. Results: Older stored red blood cells scavenge nitric oxide more than fresher cells. Conclusion: As stored red blood cells age, structural and biochemical changes occur that lead to faster scavenging. Significance: Increased nitric oxide scavenging by red blood cells as a function of storage age contributes to deleterious effects upon transfusion.

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Influence of Storage on Red Blood Cell Rheological Properties

Cited by 337 publications

References 16 publications

Storage of Red Blood Cells and Transfusion-Related Acute Lung Injury

Storage of Red Blood Cells and Transfusion-Related Acute Lung Injury

Stiffness increase of red blood cells during storage

Mechanism of Faster NO Scavenging by Older Stored Red Blood Cells

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