Abstract
Hemoglobin‐based oxygen carriers (HBOCs) with various oxygen affinities are currently being evaluated for clinical use. We tested whether HBOCs with high vs. low oxygen affinities can affect cellular oxygen uptake (VO2), using a BPAEC model.Methods:Confluent BPAECs, passages 3–6, were maintained in RPMI media, supplemented with 10% FBS, L‐glutamine, and antibiotics. 5 ×107 cells, were placed in a respirometer, containing 100μl of room air saturated buffer in the absence or presence of 1.35 g/dl HBOC‐201® (p50=26 torr @ 21.5ºC) or 1.35 g/dl HbA0 (p50= 6.9 @ 21.5ºC). Uncoupling 0.3μM carbonyl cyanide 4(tri‐fluoromethoxy) phenylhyrdrazone (FCCP) was used to trigger maximal mitochondrial VO2. The HBOC‘s oxygen dissociation curves were corrected for pH and temperature (J Appl Physiol. 94(2):561–6.2003). VO2 was defined as use of (free + bound) O2 divided by the time to full O2 depletion.Results:Untreated BPAECs had a VO2 of 3.09 ± 3.9 nmoles O2/min, which increased to 7.34 ± 5.1 with FCCP. The VO2 of BPAECs treated with HBOC‐201 was 6.69 ± 2.5 nmoles O2/min, which increased to 10.43 ± 9.1 with uncoupler. When 2,3‐DPG‐free human HbA0 was combined with FCCP the VO2 was 4.41 ± 2.3 nmoles O2/min, higher than basal control VO2 but lower than that in presence of HBOC‐201 + FCCP.Conclusion:Low oxygen affinity HBOC‐201 facilitates VO2 by BPAECS relative to high oxygen affinity HBOC preparations such as human HbA0.
Published Version
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