Kohzuki H, Enoki Y, Ohga Y, Shimizu S, Sakata S
Second Department of Physiology, Nara Medical University, Japan.
Adv Exp Med Biol. 1988;222:315-22. doi: 10.1007/978-1-4615-9510-6_37.
To clarify the influence of high O2-affinity blood on oxygen consumption by peripheral tissue, we perfused the dog gracilis muscle alternately with normal and low P50 blood at constant CaO2 and varying blood flows. VO2 was plotted against O2 delivery which was a product of CaO2 and blood flow. VO2 of the resting dog gracilis muscle was O2 delivery-dependent below a critical O2 delivery of 0.40 ml/min.100g, but became delivery-independent above this level. This relationship was essentially the same as that observed in rat skeletal muscle (Kolár and Janský, 1984), and was independent of the O2 affinity of blood, both qualitatively and quantitatively, although the PVO2 was significantly lower in the perfusions with the high affinity blood than in those with normal blood. The average PVO2 value by which the delivery-dependent and -independent VO2 regions were separated decreased from 33 Torr in the normal perfusions to 20 Torr in the high O2 affinity perfusions. In conclusion, the elevation of blood O2 affinity does not induce any reduction in VO2, and thus hypoxia, in resting skeletal muscle under normoxic conditions when O2 delivery is not below the critical level.