Systemic hemorrhage augments local O₂ extraction in canine intestine

When O₂ delivery (Q̇O₂) to a tissue is reduced, microvascular adjustments facilitate increases in O₂ extraction, thereby delaying the onset of O₂ supply limited metabolism until a critically low Q̇O₂ is reached. The present study investigated the contribution of the autonomic nervous system to these adjustments by measuring O₂ extraction in isolated intestine. In anesthetized dogs, a 30- to 50-g segment of intestine was vascularly isolated and its Q̇O₂ was decreased in stages by reducing the speed of an occlusive pump. In a normovolemic group (n = 11), blood volume was maintained to minimize sympathetic tone while flow to the intestine was reduced. In a hypovolemic group (n = 7), blood volume was removed in stages to augment sympathetic tone as flow to the intestinal segment was simultaneously reduced. A hypovolemic α-adrenergic-blocked (α-blocked) group (n = 6) was identical to the corresponding α-adrenergic intact (α- intact) group except that α-adrenergic effects were inhibited with phenoxybenzamine (3 mg/kg). The systemic critical O₂ extraction ratio in the α-blocked group (69 ± 6%) was less than that in the α-intact group (77 ± 7%; P = 0.05). In the intestine, the critical O₂ extraction ratio was significantly poorer in the normovolemic (45 ± 11%) group than in either hypovolemic group (α-intact: 69 ± 3%, P < 0.00005; α-blocked: 62 ± 9%, P < 0.005). These findings demonstrate that systemic hemorrhage significantly augments critical O₂ extraction in intestine during progressive local stagnant hypoxia and suggest that nonadrenergic vasoconstrictor mechanisms may play an important role.