Systemic and intestinal limits of O₂ extraction in the dog

When systemic delivery of O₂ (Q̇O₂ = Q̇T x Ca(O₂), where Q̇T is cardiac output and Ca(O₂) is arterial O₂ content) is reduced by bleeding, the systemic O₂ extraction ratio [ER = (Ca(O₂) - Cv(O₂)/Ca(O₂), where CV(O₂) is venous O₂ content] increases until a critical limit is reached below which O₂ uptake (V̇O₂) becomes limited by O₂ delivery. During hypovolemia, reflex increases in mesenteric arterial tone may preferentially reduce gut blood flow so that the onset of O₂ supply dependence occurs in the gut before other regions. We compared the critical O₂ delivery (Q̇O₂(c)) and critical extraction ratio (ER(c)) of whole body and an isolated segment (30-50 g) of small bowel in seven anesthetized paralyzed dogs ventilated with room air. Systemic Q̇O₂ was reduced in stages by controlled hemorrhage as arterial O₂ content was maintained, and systemic and gut V̇O₂ and Q̇O₂ were measured at each stage. Body Q̇O₂(c) was 7.9 ± 1.9 ml·kg^-1·min^-1 (ER(c) = 0.69 ± 0.12), whereas gut O₂ supply dependency occurred when gut Q̇O₂ was 34.3 ± 11.3 ml·min^-1·kg gut wt^-1 (ER(c) = 0.63 ± 0.09). O₂ supply dependency in the gut occurred at a higher systemic Q̇O₂ (9.7 ± 2.7) than whole-body Q̇O₂(c) (P < 0.05). The extraction ratio at the final stage (maximal ER) was less in the gut (0.80 ± 0.05) than whole body (0.87 ± 0.06). Thus during reductions in systemic Q̇O₂, gut V̇O₂ was maintained by increases in gut extraction of O₂. Although gut O₂ extraction at the onset of O₂ supply dependency was not worse than whole body, the gut critical point was reached at a stage when nongut V̇O₂ was still independent of supply. Hence metabolic regulation of local gut blood flow was insufficient to prevent supply limitation, despite the onset of tissue hypoxia.