• Ségolène Mrozek, Aymeric Luzi, Leslie Gonzalez, Lionel Kerhuel, Olivier Fourcade, and Thomas Geeraerts.
• Equipe d'accueil' Modélisation de l'aggression tissulaire et nociceptive', University Toulouse 3 Paul Sabatier, Toulouse, France; Departement of Anesthesiology and Critical Care, University Hospital of Toulouse, Toulouse, France. Electronic address: mrozek.s@chu-toulouse.fr.
• Brain Res. 2016 Sep 1; 1646: 334-341.

AbstractThe post-traumatic brain vulnerability suggests that after traumatic brain injury (TBI), the brain may be more susceptible to posttraumatic hypoxic insults. This concept could be extended to 'peripheral' organs, as non-neurologic organ failure is common after TBI. This study aims to characterize and quantify cerebral and extracerebral tissue hypoxia with pimonidazole resulting from a standardized hypoxia-hypotension (HH) phase occurring after a diffuse experimental TBI in rats. Rats were allocated to Sham (n=5), TBI (n=7), HH (n=7) and TBI+HH (n=7) groups. Then, pimonidazole was injected and brain, liver, heart and kidneys were analysed. In the cerebral cortex, post-treatment hypoxia was higher in TBI+HH group than Sham group (p=0.003), HH group (p=0.003) and TBI group (p=0.002). Large trends in thalamus, hippocampus and striatum for the TBI+HH group compared to the other groups were observed. For the heart and liver, the 4 groups were comparable. For the kidneys, post-treatment hypoxia was higher in the TBI group compared to the Sham and HH groups, but not more than TBI+HH group. This study reveals that a posttraumatic hypoxic insult occurring after a severe TBI has major hypoxic consequences on brain structures. However, TBI by itself appears to induce renal hypoxia that is not enhanced by posttraumatic hypoxic insult.Copyright © 2016 Elsevier B.V. All rights reserved.

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