Low-O2 affinity erythrocytes improve performance of ischemic myocardium

Abstract

O2 transport and O2 diffusion interact in providing O2 to tissue, but the extent to which diffusion may be critical in the heart is unclear. If O2 diffusion limits mitochondrial oxygenation, a change in blood O2 affinity at constant total O2 transport should alter cardiac O2consumption (V˙o 2) and function. To test this hypothesis, we perfused isolated isovolumically working rabbit hearts with erythrocytes at physiological blood-gas values and P50 (Po 2 required to half-saturate hemoglobin) values at pH of 7.4 of 17 ± 1 Torr (2,3-bisphosphoglycerate depletion) and 33 ± 5 Torr (inositol hexaphosphate incorporation). When perfused at 40 and 20% of normal coronary flow, mean V˙o 2 decreased from the control value by 37 and 46% ( P < 0.001), and function, expressed as cardiac work, decreased by 38 and 52%, respectively ( P < 0.001). Perfusion at higher P50 during low-flow ischemia improvedV˙o 2 by 20% ( P < 0.001) and function by 36% ( P < 0.02). There was also modest improvement at basal flow ( P < 0.02 and P < 0.002, respectively). The improvement inV˙o 2 and function due to the P50 increase demonstrates the importance of O2diffusion in this cardiac ischemia model.