The changes that take place in blood components during storage have long been suspected as a culprit for part of the deleterious clinical effects attributed to blood transfusion. The case against "aged" blood can be made on two fronts: the clinical (often observational) evidence linking the advanced age of blood with adverse outcomes and the laboratory (experimental) evidence showing the changes in biology, chemistry, physics, and rheology as possible mechanisms of action. In this issue of Anesthesiology, Vlaar et al. provide direct mechanistic evidence on the effect of storage of blood on lung injury and attempt to pinpoint the element(s) of blood that are adversely affected by storage and responsible for the observed harm using an animal model.
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