Adrenergic vasoconstriction augments tissue O₂ extraction during reductions in O₂ delivery

When systemic O₂ delivery is reduced, increases in systemic O₂ extraction are facilitated by sympathetically mediated increases in vascular resistance that limit blood flow to regions with low metabolic demand. Local metabolic vasodilation competes with this vasoconstriction, thereby effecting a balance between tissue O₂ supply and demand. This study examined the role of sympathetically mediated vasoconstriction on the critical level of O₂ extraction in hindlimb and whole body during progressive reductions in O₂ delivery. In anesthetized dogs, the left hindlimb was vascularly isolated and its O₂ delivery was decreased in stages by reducing the speed of an occlusive pump. In a normovolemic group (n = 6), blood volume was maintained to minimize sympathetic tone while flow to the hindlimb was reduced. In a hypovolemic group (n = 6), blood volume was removed in stages to augment sympathetic tone progressively while flow to the limb was reduced simultaneously. A phenoxybenzamine group (n = 6) was identical to the hypovolemic group, except that α-adrenergic effects were inhibited with phenoxybenzamine (3 mg/kg). The systemic critical O₂ extraction ratio in the phenoxybenzamine group (0.60 ± 0.06) was less than for the hypovolemic group (0.71 ± 0.04; P = 0.004). In the hindlimb, critical O₂ extractions were significantly less in the normovolemic (0.46 ± 0.17) and phenoxybenzamine (0.49 ± 0.10) groups compared with the hypovolemic group (0.72 ± 0.10; P ≤ 0.008). These findings demonstrate a significant contribution of α- adrenergic vasoconstrictor tone to the critical O₂ extraction in whole body and hindlimb during progressive hypoxia and underscore the significance of an active sympathetic response for efficient tissue O₂ utilization, especially in states in which O₂ delivery to an isolated region is reduced.