Increased hemoglobin-oxygen affinity does not decrease skeletal muscle oxygen consumption

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Abstract
The importance of Hb-O2 affinity (HOA) in affecting skeletal muscle O2 consumption (.ovrhdot.VO2) was reevaluted using an isolate canine gracilis muscle. HOA of the blood [normal O2 half-saturation pressure of Hb (P50) = 30 torr] was increased by refrigerated storage (P50 = 22 torr), incubation in sodium metabisulfite (P50 = 24 torr), or in sodium cyanate (P50 = 14 torr). Stored blood caused a significant fall in .ovrhdot.VO2 to 80% of control, with no change in venous O2 partial pressure (PVO2), substantiating previous studies. In contrast, blood incubated in sodium metabisulfite or sodium cyanate resulted in no impairment of .ovrhdot.VO2, with a fall in PVO2 in the latter case indicating that a critical PVO2 did not cause the reduction in .ovrhdot.VO2 with stored blood. To substantiate further the lack of existence of a critical PO2, fresh and increased HOA blood was perfused at constant flow rates and varying arterial O2 saturations. Stored blood showed a marked reduction in .ovrhdot.VO2 as compared with normal blood over a wide range of saturations. Carbamylated blood .ovrhdot.VO2 was identical to fresh blood .ovrhdot.VO2 values. The position of the O2 dissociation curve may not be as important as originally thought in determining skeletal muscle O2 delivery. The drop in .ovrhdot.VO2 caused by perfusion with stored blood is due to some other factor unrelated to HOA.

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