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Editorial
. 2012 Jul;52(7):1388-92.
doi: 10.1111/j.1537-2995.2012.03748.x.

Nitric oxide, hemolysis, and the red blood cell storage lesion: interactions between transfusion, donor, and recipient

Editorial

Nitric oxide, hemolysis, and the red blood cell storage lesion: interactions between transfusion, donor, and recipient

Tamir Kanias et al. Transfusion. 2012 Jul.
No abstract available

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Figures

Figure 1
Figure 1
Donor genetic variation including gender can affect hemolytic propensity and red cell storage recovery. The red cell storage lesion can involve modifications in membrane structure leading to the release of microparticles and hemolysis. Massive transfusions of red cell units or transfusion into patients suffering endothelial dysfunction, infection, and other pathological situations (susceptible hosts) can exacerbate inflammation, vasoconstriction and hypertension leading to multiple organ dysfunction syndrome (MODS). Additionally, hemolysis can exacerbate sepsis by the release of iron from denatured hemoglobins. Nitric oxide therapeutics can potentially mitigate transfusion-related injuries in patients suffering endothelial dysfunction by improving NO bioavailability required for vasodilation and proper endothelial function.

Comment on

References

    1. Baek JH, D’Agnillo F, Vallelian F, Pereira CP, Williams MC, Jia Y, Schaer DJ, Buehler PW. Hemoglobin-driven pathophysiology is an in vivo consequence of the red blood cell storage lesion that can be attenuated in guinea pigs by haptoglobin therapy. J Clin Invest. 2012;122:1444–58. - PMC - PubMed
    1. Beutler E, Kuhl W, West C. The osmotic fragility of erythrocytes after prolonged liquid storage and after reinfusion. Blood. 1982;59:1141–7. - PubMed
    1. Donadee C, Raat NJ, Kanias T, Tejero J, Lee JS, Kelley EE, Zhao X, Liu C, Reynolds H, Azarov I, Frizzell S, Meyer EM, Donnenberg AD, Qu L, Triulzi D, Kim-Shapiro DB, Gladwin MT. Nitric oxide scavenging by red blood cell microparticles and cell-free hemoglobin as a mechanism for the red cell storage lesion. Circulation. 2011;124:465–76. - PMC - PubMed
    1. Gabrio BW, Finch CA. Erythrocyte preservation. I. The relation of the storage lesion to in vivo erythrocyte senescence. J Clin Invest. 1954;33:242–6. - PMC - PubMed
    1. Gladwin MT, Kim-Shapiro DB. Storage lesion in banked blood due to hemolysis-dependent disruption of nitric oxide homeostasis. Curr Opin Hematol. 2009;16:515–23. - PubMed

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