Muscle O₂ Uptake While Perfused at Constant Pressure with Normoxic Blood During Global Hypoxia

Abstract

When the isolated hindlimb muscles of anesthetized dogs were perfused at constant flow (CF) with normoxic blood while the whole animal was ventilated with 9% O₂ in N₂, limb O₂ uptake (VO₂) increased 25% instead of decreasing with whole body VO₂ (Bredle et al., 1988a). This hypoxia-induced increase in limb O₂ demand was attributed to the calorigenic effects of catecholamines liberated at sympathetic nerve endings and from the adrenal medulla as a result of increased chemoreceptor activity during hypoxia (Blatteis and Lutherer, 1974; Cain, 1969; Sylvester et al., 1979). The increase in hindlimb VO₂ was prevented by β₂-adrenergic receptor blockade (Bredle et al., 1988a) and was largely dependent on intact innervation to the hindlimb (Bredle et al., 1988b). Our goal in the present study was two-fold: 1) to ascertain whether hypoxic vasoconstrictor tone was sufficiently potent to prevent any increase in limb VO₂ even if it were perfused with normoxic blood, and 2) to observe whether any autoregulatory escape would occur if that were the case. With respect to the second goal, as the ratio of O₂ supply to demand decreases, then local vasodilator factors should accumulate to relieve local vasoconstriction (Cain and Chapler, 1979). To accomplish these goals, we pump-perfused the limb muscles of anesthetized dogs with normoxic blood at constant perfusion pressure (CP) while ventilating them with an hypoxic gas mixture. In this manner, blood flow varied inversely with the level of sympathetic vasoconstrictor tone.