Carbon dioxide reactivity and pressure autoregulation of brain tissue oxygen

OBJECTIVE: To describe the normal relationships between brain tissue oxygen tension (PbrO₂) and physiological parameters of systemic blood pressure and CO₂ concentrations. METHODS: Licox Clark-type oxygen probes (GMS mbH, Kiel, Germany) were inserted in the frontal white matter of 12 swine maintained under general anesthesia with a 1.0 fraction of inspired oxygen (FiO₂). In seven swine, alterations in end-tidal carbon dioxide (ET-CO₂) concentration (range, 13-72 mm Hg) were induced via hyperventilation or instillation of CO₂ into the ventilation circuit. In nine swine, mean arterial pressure (MAP) (range, 33-200 mm Hg) was altered; phenylephrine was used to induce hypertension, and a nitroprusside-esmolol combination or systemic hemorrhage was used for hypotension. Quantitative cerebral blood flow (CBF) was measured in two animals by using a thermal diffusion probe. RESULTS: Mean baseline PbrO₂ was 41.9 ± 11.3 mm Hg. PbrO₂ varied linearly with changes in ET-CO₂, ranging from 20 to 60 mm Hg (r² = 0.70). The minimum PbrO₂ with hypocarbia was 5.9 mm Hg, and the maximum PbrO₂ with hypercarbia was 132.4 mm Hg. PbrO₂ varied with MAP in a sigmoid fashion suggestive of pressure autoregulation between 60 and 150 mm Hg (r² = 0.72). The minimum PbrO₂ with hypotension was 1.4 mm Hg, and the maximum PbrO₂ with hypertension was 97.2 mm Hg. In addition, CBF correlated linearly with PbrO₂ during CO₂ reactivity testing (r² = 0.84). CONCLUSION: In the uninjured brain, PbrO₂ exhibits CO₂ reactivity and pressure autoregulation. The relationship of PbrO₂ with ET-CO₂ and MAP appears to be similar to those historically established for CBF with ET-CO₂ and MAP. This suggests that, under normal conditions, PbrO₂ is strongly influenced by factors that regulate CBF.