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Attenuated erythrocytic ATP release is caused by extracellular hemoglobin.
Author(s) -
Cole Russell H,
Malavalli Ashok,
Vandegriff Kim D
Publication year - 2009
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.23.1_supplement.lb65
Subject(s) - extracellular , chemistry , hemoglobin , luciferin , intracellular , vasodilation , biochemistry , oxygen , luciferase , extracellular fluid , biophysics , endocrinology , biology , transfection , organic chemistry , gene
Local regulation of microvascular flow is a complex process evolved to match oxygen supply to the metabolic demands of the tissue. The RBC has been proposed as an O 2 sensor through a direct link between the desaturation of intracellular hemoglobin (Hb) and ATP release, leading to vasodilation 1 . This theory suggests a link between alterations of O 2 transport parameters in the plasma space and vasoactivity. Based on theoretical calculations of O 2 extraction from RBCs in the presence of Hb‐based oxygen carriers (HBOCs), we hypothesized that that the addition of cell‐free Hb to the extracellular space provides a supplementary O 2 source that reduces RBC desaturation and ATP release. In this study, the total O 2 concentration of RBC/HBOC suspensions was lowered by additions of deoxygenated saline, and then assayed for ATP production via the luciferin‐luciferase bioluminescence assay. When an acellular Hb cross‐linked between α subunits (αα Hb, p50 = 33 mmHg) was added to the red cell suspension, ATP production was significantly less in the absence of HBOC. These results provide a possible mechanism for HBOC‐induced vasoactivity through delayed release of red cell ATP. 1 Ellsworth, ML (2000) Acta Physiol Scand 168: 551‐559.