To determine the role of arterial O2 content (Ca(O2)) in the cerebral flow (CBF) responses to hypoxemia and hemodilution. Ca(O2) was progressively reduced from ≃ 18 to ≃ 6 ml O2/dl in normocapnic, normothermic, pentobarbital-anesthetized rabbits. This was done either by reducing Pa(O2) (hypoxemia, minimum Pa(O2) ≃ 26 mmHg) or arterial hematocrit (isovolemic hemodilution with hetastarch, minimum hematocrit ≃ 14%) while CBF was measured with radioactive microspheres. As Ca(O2) decreased, CBF increased in both groups but was greater in hypoxemic animals at Ca(O2) values ≤ 9 ml O2/dl. For example, at a Ca(O2) ≃ 6 ml O2/dl, CBF in hypoxemic animals was 110 ± 38 ml · 100 g-1 · min-1 (means ± SD) compared with 82 ± 22 ml · 100 g-1 · min-1 in hemodiluted animals (means ± SD). While calculated cerebral O2 delivery (cerebral DO2) was well maintained in hypoxemic animals, it decreased significantly during hemodilution (from 7.95 ± 2.92 baseline to 5.08 ± 1.10 ml O2/dl · 100 g-1 · min-1 at the lowest Ca(O2) value). This decrease in cerebral DO2 was offset by an increase in oxygen extraction ratio during hemodilution. By contrast, the small increase in oxygen extraction ratio seen with hypoxemia did not achieve significance. These results suggest that there are different adaptive responses to acute hypoxemia or hemodilution. They also imply that at similar CBF and Ca(O2) values, tissue O2 availability may be greater during hemodilution than during hypoxemia.
|Original language||English (US)|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|Issue number||5 36-5|
|State||Published - 1994|
- cerebral oxygen consumption