Carbon dioxide reactivity and pressure autoregulation of brain tissue oxygen

OBJECTIVE: To describe the normal relationships between brain tissue oxygen tension (PbrO(2)) 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 (FiO(2)). 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 PbrO(2) was 41.9 +/- 11.3 mm Hg. PbrO(2) varied linearly with changes in ET-CO2, ranging from 20 to 60 mm Hg (r(2) = 0.70). The minimum PbrO(2) with hypocarbia was 5.9 mm Hg, and the maximum PbrO(2) with hypercarbia was 132.4 mm Hg. PbrO(2) varied with MAP in a sigmoid fashion suggestive of pressure autoregulation between 60 and 150 mm Hg (r(2) = 0.72). The minimum PbrO(2) with hypotension was 1.4 mm Hg, and the maximum PbrO(2) with hypertension was 97.2 mm Hg. In addition, CBE correlated linearly with PbrO(2) during CO2 reactivity testing (r(2) = 0.84). CONCLUSION: In the uninjured brain, PbrO(2) exhibits CO2 reactivity and pressure autoregulation. The relationship of PbrO(2) 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, PbrO(2) is strongly influenced by factors that regulate CBF.