After traumatic brain injury (TBI), lesions are anatomically heterogeneous, but the spatial heterogeneity of the post-traumatic brain's vulnerability to hypoxia-hypotension (HH) has been poorly studied. Our objective was to compare the effect of HH after TBI on brain energy metabolism into two regions: the frontal lobe and the thalamus. Twenty-eight Sprague-Dawley rats were randomized into four groups: sham, TBI (brain trauma alone, impact acceleration, 450-g weight drop from 1.8m), HH (blood depletion to mean arterial pressure 40mm Hg, FiO2 10%, 15min), and TBI-HH (TBI followed by HH, 45-min delay). Cerebral perfusion pressure (CPP) was continuously measured. Brain microdialysis and brain tissue oxygen partial pressure (PtiO2) probes were both inserted stereotaxically into the right thalamus and frontal lobe. Except during the HH period, CPP was always above 60mm Hg. During the hour following the HH period, significant increases in cerebral lactate-pyruvate ratio, glycerol, and glutamate were observed, and were always higher in the frontal lobe than in the thalamus (p<0.001). In the TBI-HH group and in the frontal lobe, increases in glutamate and glycerol were significantly higher than in the HH group (p<0.001). During the 30min following the HH phase (reperfusion), an increase in PtiO2 was observed. In the TBI-HH group, this increase was significantly lower in the frontal lobe than in the thalamus. These findings demonstrate that in the early post-traumatic period, the metabolic cerebral response to HH is higher in the frontal lobe than in the thalamus, and is worsened by TBI, suggesting a higher vulnerability for the frontal lobes.
- energy metabolism
- traumatic brain injury