In their complex basic science work, the authors suggest that NO signaling plays a central role in the transfusion-related injury observed in critically ill patients, especially in trauma patients with massive transfusion. They observed increased NO scavenging by hemoglobin in human leukocyte-depleted RBCs after 14 days of storage. This modification of NO availability may contribute to the inhibition of NO-dependent vasodilatation observed after incubation of such erythrocytes on rat aorta. The hypothesis here is that modifications of red blood cell shape, size and membrane during storage could limit the diffusion of NO from the erythrocyte to the vessel. Nevertheless, extrapolation of these ex-vivo results to the clinical situation remains difficult. Indeed, concentrations of free hemoglobin and microparticles also increased during storage and in trauma patients. All could also have induced the same modifications on NO metabolism. This point could limit the results of this study.
– Michael Piagnerelli