Oxygen delivery and uptake in dogs during anemic and hypoxic hypoxia.
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.
Oxygen delivery and uptake in dogs during anemic and hypoxic hypoxia. 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.