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Impact of Augmenting Intracellular ATP on the Inducible Release of ATP from Banked Erythrocytes
Author(s) -
Kirby Brett S,
Zhu Hongmei,
Riccio Daniel A,
McMahon Timothy J
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1147.3
Subject(s) - intracellular , extracellular , adenosine triphosphate , chemistry , biophysics , biochemistry , biology
Prolonged banking of human erythrocytes (RBCs) coincides with adverse clinical outcomes following blood transfusion. Healthy RBCs release ATP that is vasoactive and anti‐adhesive, but hypoxia‐induced release of ATP from banked RBCs is markedly impaired. We tested the hypothesis that stored RBCs (35–42 days in blood bank) demonstrate impairments in ATP release that are common among disparate stimuli, and that release can be improved with an intracellular ATP ([ATP] i ) boosting solution (Rejuvesol). ATP release from human RBCs (fresh or stored) was measured after mechanical deformation (5μm filtration) or direct G‐protein activation (mastoparan7; Mas7). Average basal ATP release was 146±19 and 107±14 nM from fresh and stored RBCs, respectively. Deformation‐induced release from stored RBCs was blunted compared to fresh (Δ34 vs 180%), but similar from Mas7 (Δ78 vs 95%). [ATP] i was lower in stored vs fresh RBCs, but elevated by Rejuvesol (2.8 vs 4.8 vs 6.8 umol/g Hb). Augmenting [ATP] i increased ATP release upon deformation by 2‐fold, but had no impact on Mas7‐induced release. These data suggest a specific impairment in inducible ATP release from stored human RBCs that is upstream of G‐protein coupled receptor activation, and that augmenting [ATP] i may improve ATP release in response to deformation. Improved ATP export may in turn support better clinical outcomes following RBC transfusion. Support NIH HL113943