Brain Oxygen Tension,Oxygen Supply,and Oxygen Consumption During Arterial Hyperoxia in a Model of Progressive Cerebral Ischemia

Abstract

We investigated the changes in brain oxygen tension (ptiO₂) after ventilation with pure O₂ in order to (1) clarify the pathophysiology of O₂ exchange in the cerebral microcirculation; and (2) investigate the relationship between brain O₂ tension, O₂ delivery, and consumption in steady-state conditions during stepwise cerebral blood flow (CBF) reductions. A swine model was developed to reduce CBF in three stable steps: (1) baseline (CBF 100%), (2) CBF of 50-60% of baseline, and (3) CBF of < 30% of baseline. CBF was reduced by infusing saline into the left lateral ventricle through a catheter connected with an infusion pump. At each step, hyperoxia was tested by increasing the inspired oxygen fraction up to 100%, PtiO₂ reflected the CBF reductions, since it was respectively 27.95 (± 10.15), 14.77 (± 3.58), and 3.45 (± 2.89) mm Hg during the three CBF steps. Hyperoxia was followed by an increase in ptiO₂, although the increase was significantly lower when hyperoxia was applied during progressive ischemia. O₂ supply to the brain did not change during hyperoxia. Arteriovenous oxygen difference (AVDO₂) decreased during the phases of intact CBF and moderate impairment, but not during the phase of severe CBF reduction. In conclusion, ptiO₂ reductions closely reflect the imbalance between oxygen delivery and demand; this implies a link between low ptiO₂ and defective O₂ supply due to impaired CBF. However, this relation is not necessarily reciprocal, since manipulating brain oxygen tension does not always influence brain oxygen delivery, as in the case of ventilation with pure oxygen.