ADRENERGIC VASOCONSTRICTION AUGMENTS TISSUE O-2 EXTRACTION DURING REDUCTIONS IN O-2 DELIVERY

When systemic O-2 delivery is reduced, increases in systemic O-2 extra ction are facilitated by sympathetically mediated increases in vascula r resistance that limit blood flow to regions with low metabolic deman d. Local metabolic vasodilation competes with this vasoconstriction, t hereby effecting a balance between tissue O-2 supply and demand. This study examined the role of sympathetically mediated vasoconstriction o n the critical level of O-2 extraction in hindlimb and whole body duri ng progressive reductions in O-2 delivery. In anesthetized dogs, the l eft hindlimb was vascularly isolated and its O-2 delivery was decrease d in stages by reducing the speed of an occlusive pump. In a normovole mic 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 phe noxybenzamine group (n = 6) was identical to the hypovolemic group, ex cept that alpha-adrenergic effects were inhibited with phenoxybenzamin e (3 mg/kg). The systemic critical O-2 extraction ratio in the phenoxy benzamine group (0.60 +/- 0.06) was less than for the hypovolemic grou p (0.71 +/- 0.04; P = 0.004). In the hindlimb, critical O-2 extraction s were significantly less in the normovolemic (0.46 +/- 0.17) and phen oxybenzamine (0.49 +/- 0.10) groups compared with the hypovolemic grou p (0.72 +/- 0.10; P less than or equal to 0.008). These findings demon strate a significant contribution of alpha-adrenergic vasoconstrictor tone to the critical O-2 extraction in whole body and hindlimb during progressive hypoxia and underscore the significance of an active sympa thetic response for efficient tissue O-2 utilization, especially in st ates in which O-2 delivery to an isolated region is reduced.