Background and aim: Using broadband near-infrared spectroscopy (BBS), we have previously demonstrated an increase in aerobic metabolism in the human healthy brain following hypercapnea and hyperoxia. 1 We also observed oxidation in cerebral cellular and mitochondrial redox states, using cerebral microdialysis (MD) and BBS respectively, following hyperoxia in patients with traumatic brain injury (TBI). 2 In this study we investigate the effect of hypercapnea on regional metabolism in the injured brain using BBS and MD. Methods: Following ethics approval and assent from nominated representatives, 6 sedated patients with severe TBI were studied 3-5 days after injury. Cerebral blood flow velocity (Vmca) was measured using transcranial Doppler ultrasonography. Changes in cellular and mitochondrial redox state were measured from the changes in brain tissue lactate and pyruvate concentration using MD and the change in oxidized cytochrome c oxidase concentration ([oxCCO]) using BBS.[oxCCO] was measured in a region of interest adjacent to the site of the MD catheter. Intracranial pressure (ICP) was also monitored continuously. During a period of cardiovascular stability, the rate of mechanical ventilation was reduced in a stepwise manner to produce an increase in PaCO 2 of approximately 1.5kPa. Changes in the continuously measured variables ([oxCCO], ICP and Vmca) during hypercapnea were compared with baseline values using a Student's paired t-test (significance at P < 0.05).Results: In all patients hypercapnea caused a significant increase in Vmca and ICP. Analysis of the BBS data demonstrated two patterns of [oxCCO] change in response to hypercapnea, Group A showing a significant increase in [oxCCO] and Group B a significant decrease (P < 0.05).
Conclusions:In our previous study in TBI, hyperoxia resulted in an increase in [oxCCO] in all patients, consistent with an increase in aerobic metabolism secondary to the induced increase in cerebral oxygen delivery. 2 Hypercapnea can also increase cerebral oxygen delivery via an increase in cerebral blood flow. In this study Vmca increased in all patients during hypercapnea. However despite the likely increase in cerebral oxygen delivery, we did not see an increase in the oxidation status of [oxCCO] in every patient. Interestingly, changes in MD measured metabolic variables were similar in all patients. Further work is required to determine why the continuous optically measured metabolic variable was able to identify two distinct patterns of change in [oxCCO] in response to hypercapnea whereas the non continuous MD variables were not.