When the delivery of O2 to tissues (Q̇O2 = blood flow x O2 content) falls below a critical threshold, tissue O2 uptake (V̇O2) becomes limited by Q̇O2. The mechanism responsible for this extraction limitation is not understood but may involve molecular diffusion limitation as mean capillary PO2 drops below a critical minimum level in some capillaries. We tested this hypothesis by measuring the critical Q̇O2 necessary to maintain V̇O2 independent of Q̇O2 in anesthetized, paralyzed normal dogs (n = 7) and in a second group in which PO2 at 50% saturation of hemoglobin (P50) was reduced by exchange transfusion with low-P50 erythrocytes (n = 7). Q̇O2 was reduced in stages by removing blood volume to reduce blood flow while V̇O2 was measured by spirometry at each step. To the extent that O2 extraction was limited by a critical capillary PO2, we reasoned that the onset of diffusion limitation should occur at a higher Q̇O2 with low P50, since a lower end-capillary PO2 is required to achieve the same O2 extraction. The critical Q̇O2 (7.8 ± 1.2 ml·min-1·kg-1) and extraction ratio (0.63 ± 0.06) in dogs with reduced P50 were not different from controls. At the critical delivery, mixed venous PO2 was lower in low P50 (16.1 ± 2.9 Torr) than controls (29.9 ± 2.3 Torr). We conclude that diffusion limitation does not initiate the early fall in V̇O2 below the critical Q̇O2 and offer an alternative model to explain the onset of supply dependency. Dogs with normal P50 achieved higher maximal extractions at the end of the study than low P50 animals (P < 0.01) suggesting that low P50 does confound O2 extraction when delivery is very low.
ASJC Scopus subject areas
- Physiology (medical)