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Crit Care. 2010; 14(Suppl 1): P296.
Published online 2010 March 1. doi:  10.1186/cc8528
PMCID: PMC2934392

Cortex and deep grey matter have different sensitivities to hypoxia-hypotension and traumatic brain injury: a combined PtiO2 and microdialysis study in rats

Introduction

After traumatic brain injury (TBI), structural lesions are heterogeneous, but the spatial heterogeneity of consequences of insults as hypoxia-hypotension (HH) and/or TBI has never been studied. The objective of this study was to compare the effect of standardized insults (HH, TBI and both) on brain energy metabolism in two different regions: frontal cortex and thalamus.

Methods

Twenty-eight Sprague-Dawley rats were randomized into four groups: Sham, TBI (impact acceleration alone, 450 g weight drop from 1.8 m), HH (blood depletion to mean arterial pressure 40 mmHg, FiO2 10%, 15 minutes) and TBI-HH (TBI followed by HH, 45 minute delay). Cerebral perfusion pressure (CPP) was continuously and invasively measured. Brain microdialysis and PtiO2 probes were both inserted stereotaxically in the right thalamus and frontal cortex.

Results

Except during the HH phase, CPP was always greater than 60 mmHg. During the hour following the HH period, a significant increase in cerebral lactate/pyruvate ratio (Figure (Figure1),1), glycerol and glutamate was observed. This increase was higher in the cortex than in the thalamus in all groups subjected to HH (P < 0.001). In the TBI-HH groups, the increase in glycerol in the cortex was significantly higher compared with the HH group (P < 0.001), as well as thalamic and cortical glutamate. During 15 minutes following the HH phase (after reinjection and reoxygenation), an increase in PtiO2 was observed in the cortex and thalamus, but with different profiles (lower increase in the cortex) (Figure (Figure11).

Figure 1
Brain lactate/pyruvate ratios and PtiO2 in the thalamus and cortex.

Conclusions

Different profiles of cerebral response to HH and TBI were observed with higher sensitivity in the cortex than in the thalamus. The post-ischemic hyperemia seems to be altered in the traumatized cortex but conserved into the thalamus and nontraumatized brain.


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