Storage lesion: role of red blood cell breakdown - PubMed (original) (raw)

Storage lesion: role of red blood cell breakdown

Daniel B Kim-Shapiro et al. Transfusion. 2011 Apr.

Abstract

As stored blood ages intraerythrocytic energy sources are depleted resulting in reduced structural integrity of the membrane. Thus, stored red blood cells (RBCs) become less deformable and more fragile as they age. This fragility leads to release of cell-free hemoglobin (Hb) and formation of microparticles, submicron Hb-containing vesicles. Upon transfusion, it is likely that additional hemolysis and microparticle formation occurs due to breakdown of fragile RBCs. Release of cell-free Hb and microparticles leads to increased consumption of nitric oxide (NO), an important signaling molecule that modulates blood flow, and may promote inflammation. Stored blood may also be deficient in recently discovered blood NO synthase activity. We hypothesize that these factors play a potential role in the blood storage lesion.

© 2011 American Association of Blood Banks.

PubMed Disclaimer

Conflict of interest statement

JL declares no conflict of interest.

Figures

Figure 1

Figure 1

Proposed mechanisms contributing to the storage lesion. Reprinted by permission from Macmillan Publishers Ltd:Nature Medicine (16(4):381-2), copyright (2010). Red cell breakdown leads to release of cell-free hemoglobin and red cell microparticles. These scavenge NO which leads to vasoconstriction, platelet activation and adhesion, and inflammatory pathways.

Figure 2

Figure 2

General hypothesis and approach. Loss of red cell integrity during storage or upon transfusion (to be studied in Aim 1) results in release of free hemoglobin and red cell microparticles which scavenge nitric oxide leading to deleterious effects including susceptibility to platelet activation, inflammation, and poor control of blood flow. This loss of NO bioavailability may also be exacerbated by loss of red cell NOS activity, to be studied as part of Aim 2. In order to counteract these effects, in Aim 3, we will explore ways to reduce red cell breakdown during storage, reduce NO scavenging when there is red cell breakdown, and compensate for loss of NO activity using various donor substances.

Similar articles

Cited by

References

    1. Dern RJ, Brewer GJ, Wiorkowski JJ. Studies on the preservation of human blood. II. The relationship of erythrocyte adenosine triphosphate levels and other in vitro measures to red cell storageability. J Lab Clin Med. 1967;69:968–78. - PubMed
    1. Silliman CC, Clay KL, Thurman GW, et al. Partial Characterization of Lipids That Develop During the Routine Storage of Blood and Prime the Neutrophil Nadph Oxidase. Journal of Laboratory and Clinical Medicine. 1994;124(5):684–94. - PMC - PubMed
    1. Beutler E, Kuhl W. Volume Control of Erythrocytes During Storage - the Role of Mannitol. Transfusion. 1988;28(4):353–7. - PubMed
    1. Latham JT, Bove JR, Weirich FL. Chemical and Hematologic Changes in Stored Cpda-1 Blood. Transfusion. 1982;22(2):158–9. - PubMed
    1. Greenwalt TJ, Sostok CZ, Dumaswala UJ. Studies in Red-Blood-Cell Preservation .2. Comparison of Vesicle Formation, Morphology, and Membrane-Lipids During Storage in as-1 and Cpda-1. Vox Sanguinis. 1990;58(2):90–3. - PubMed

Publication types

MeSH terms

Substances

LinkOut - more resources