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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.

Unlabelled: Arterial hyperoxia improves oxygen tension measured into the cerebral tissue (ptiO2). The extent of this improvement in ameliorating O2 delivery to the cerebral tissue, when cerebral blood flow (CBF) is reduced, is still unclear. The present experiment was developed to investigate the effect of arterial hyperoxia at normal or reduced CBF (baseline, CBF = 50-60%, and CBF = 20-30% of the baseline). CBF reduction was achieved in 7 pigs by saline infusion in a lateral ventricle. PtiO2 was measured by Licox equipment. Arterovenous oxygen difference (AVDO2) was calculated as the difference between arterial oxygen content and superior sagittal sinus oxygen content. Hyperoxia was induced by increasing inspired oxygen fraction to 100%. PtiO2 moved respectively from 27.95 (+/- 10.15) to 45.98 (+/- 15.31), from 14.77 (+/- 3.58) to 30.71 (+/- 12.2), and from 3.45 (+/- 2.89) to 11.1 (+/- 12.6) mmHg at normal CBF, after the first reduction and after the second reduction. O2 supply showed only a negligible increase. AVDO2 decreased during the phases of intact and moderate CBF impairment, while it did not change during the phase of severe CBF impairment., In Conclusion: an increase of ptiO2 does not necessarily correspond to an improvement of brain oxygen delivery. The small increase in oxygen delivery due to hyperoxia may cause a slight improvement in the balance between O2 delivery and consumption during mild CBF reduction, but such improvement is negligible when severe CBF reduction occurs.

Unlabelled: Interest in tissue oxygen (PtiO2) monitoring is increasing. However the exact interactions between ptiO2, systemic and cerebral variables are a matter of debate. Particularly, the relationship between ptiO2, cerebral oxygen supply and consumption needs to be clarified. We designed a model to achieve progressive Cerebral Blood Flow (CBF) reduction through 3 steps: 1. baseline, 2. CBF between 50-60% of the baseline, 3. CBF < 30% of the baseline. In 7 pigs, under general anaesthesia, Cerebral Perfusion Pressure (CPP) and CBF were reduced through the infusion of saline in a lateral ventricle. PtiO2 and CBF were monitored respectively through a Clark electrode (Licox, GMS) and laser doppler (Peri-Flux). Blood from superior sagittal sinus and from an arterial line was simultaneously drawn to calculate the artero-venous difference of oxygen (AVDO2). Brain oxygen supply was calculated by multiplying relative CBF change and arterial oxygen content. PtiO2 reflected CBF reductions, as it was 27.95 (+/- 10.15) mmHg during the first stage of intact CBF, declined to 14.77 (+/- 3.58) mmHg during the first CBF reduction, declined to 3.45 (+/- 2.89) mmHg during the second CBF reduction and finally fell to 0 mmHg when CBF was completely abolished. CBF changes were also followed by a decline in O2 supply and a parallel increase in AVDO2., Conclusion: This model allows stable and reproducible steps of progressive CBF reduction in which ptiO2 changes can be studied together with oxygen supply and consumption.