Red blood cell (RBC) transfusion is indicated to improve oxygen delivery to tissue, and for no other purpose. We have come to appreciate that donor RBCs are fundamentally altered during processing and storage in a manner that both impairs oxygen transport efficacy and introduces additional risk by perturbing both immune and coagulation systems. The protean biophysical and physiological changes in RBC function arising from storage are termed the "storage lesion;" many have been understood for some time; for example, we know that the oxygen affinity of stored blood rises during the storage period and that intracellular allosteric regulators, notably 2,3-bisphosphoglyceric acid and ATP, are depleted during storage. Our appreciation of other storage lesion features has emerged with improved understanding of coagulation, immune, and vascular signaling systems. Here, we review key features of the "storage lesion." Additionally, we call particular attention to the newly appreciated role of RBCs in regulating linkage between regional blood flow and regional O(2) consumption by regulating the bioavailability of key vasoactive mediators in plasma, and discuss how processing and storage disturb this key signaling function and impair transfusion efficacy.
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