To test the role of blood flow in tissue hypoxia-related increased veno-arterial PCO(2) difference (DeltaPCO(2)), we decreased O(2) delivery (&Ddot;O(2)) by either decreasing flow [ischemic hypoxia (IH)] or arterial PO(2) [hypoxic hypoxia (HH)] in an in situ, vascularly isolated, innervated dog hindlimb perfused with a pump-membrane oxygenator system. Twelve anesthetized and ventilated dogs were studied, with systemic hemodynamics maintained within normal range. In the IH group (n = 6), hindlimb DO(2) was progressively lowered every 15 min by decreasing pump-controlled flow from 60 to 10 ml. kg(-1). min(-1), with arterial PO(2) constant at 100 Torr. In the HH group (n = 6), hindlimb DO(2) was progressively lowered every 15 min by decreasing PO(2) from 100 to 15 Torr, when flow was constant at 60 ml. kg(-1). min(-1). Limb DO(2), O(2) uptake (VO(2)), and DeltaPCO(2) were obtained every 15 min. Below the critical DO(2), VO(2) decreased, indicating dysoxia, and O(2) extraction ratio (VO(2)/DO(2)) rose continuously and similarly in both groups, reaching a maximal value of approximately 90%. DeltaPCO(2) significantly increased in IH but never differed from baseline in HH. We conclude that absence of increased DeltaPCO(2) does not preclude the presence of tissue dysoxia and that decreased flow is a major determinant in increased DeltaPCO(2).

Three groups of dogs were anesthetized, paralyzed, and ventilated at constant rates with the spleen clamped. Two groups were isovolemically hemodiluted with warm dextran and plasma to hematocrits just above and below that at which O2 uptake (VO2) could not be maintained at preanemic levels. One of these groups was given propranolol to reduce the cardiac output response to anemia. The third group was ventilated on a low O2 gas mixture to decrease oxygen uptake. VO2 was thus limited at a high-delivery O2 pressure (PO2) in anemia and a low-delivery PO2 in hypoxic hypoxia. VO2 was reduced at a mixed venous PO2 of 45 Torr in anemia and at 17 Torr in hypoxic hypoxia. VO2, mixed venous PO2, and O2 delivery decreased precipitously at hematocrits below 10%. Once VO2 was limited by O2 availability, a single linear relationship (r = 0.91) was found for percent VO2 as a function of total O2 delivery (cardiac output X arterial O2 content) during both anemic and hypoxic hypoxia. The critical value for O2 delivery was 9.8 ml/kg-min. When O2 supply became limiting, VO2 apparently was not diffusion limited because it was more dependent on volume delivery rates than on delivery PO2.

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Background: We studied human locomotor adaptation to powered ankle-foot orthoses with the intent of identifying differences between two different orthosis control methods. The first orthosis control method used a footswitch to provide bang-bang control (a kinematic control) and the second orthosis control method used a proportional myoelectric signal from the soleus (a physiological control). Both controllers activated an artificial pneumatic muscle providing plantar flexion torque.