Article summary: Improving the quality of banked blood
A very interesting article from Duke university on restoring the RBC deformability and reducing endothelium adhesion of banked blood.
Banked blood is widely used for blood transfusion to replace lost or malfunctioning red blood cells. Banked blood is known to have a very limited shelf life due to storage lesions. These lesions are actually already induced in the first hours of storage. Normal RBC’s circulate for some 100 days in the human body before being recycled. Banked transfusion RBC’s in contrast are known to have a half-life of only 7 to 10 days. This short half-life and transfusion related complications can be anticipated from the (Lorrca) measured reduction in deformability and increase in endothelial adhesion of the RBC’s.
This study shows that storage lesions of the banked RBC (in an animal model) may be reversed, prior to transfusion, by reloading the RBC’s with NO. Interestingly for me as a mechanical engineer the S-nitrosylation also seems to lubricate the RBC’s cytoskeleton.
Renitrosylation of banked human red blood cells improves deformability and reduces adhesivity.
Article in Transfusion · June 2015
Daniel A Riccio, Hongmei Zhu, Matthew W Foster, Brendan Huan, Christina Hofmann, Gregory M Palmer
Abstract
Transfusion of red blood cells (RBCs) is a frequent health care practice. However, unfavorable consequences may occur from transfusions of stored RBCs and are associated with RBC changes during storage. Loss of S-nitrosohemoglobin (SNO-Hb) and other S-nitrosothiols (SNOs) during storage is implicated as a detriment to transfusion efficacy. It was hypothesized that restoring SNOs within banked RBCs would improve RBC functions relevant to successful transfusion outcomes, namely, increased deformability and decreased adhesivity.
Stored human RBCs were incubated with nitric oxide (NO) donors PROLI/NO and DEA/NO (disodium 1-[2-(carboxylato)-pyrrolidin-1-yl]diazen-1-ium-1,2-diolate and diethylammonium (Z)-1-(N,N-diethylamino)diazen-1-ium-1,2-diolate) under varying experimental conditions (e.g., aerobic/anaerobic incubation, NO donor to RBC ratio). SNO restoration was evaluated in vitro and in vivo as a means to improve RBC function after storage.
Incubation of RBCs with the NO donors resulted in 10-fold greater levels of SNO-Hb versus untreated control or sham RBCs, with significantly higher Hb-bound NO yields from an NO dose delivered by DEA/NO. RBC incubation with DEA/NO at a stoichiometry of 1:62.5 NO:Hb significantly increased RBC deformabilty and reduced adhesion to cultured endothelial cells. RBC incubation with DEA/NO also increased S-nitrosylation of RBC cytoskeletal and membrane proteins, including the β-spectrin chain. Renitrosylation attenuated both RBC sequestration in the lung and the mild blood oxygen saturation impairments seen with banked RBCs in a mouse model of transfusion.
RBC renitrosylation using NO donors has promise for correcting deficient properties (e.g., adhesivity, rigidity, and SNO loss) of banked RBCs and in turn improving transfusion outcomes.