Mannitol improves brain tissue oxygenation in a model of diffuse traumatic brain injury

Clotilde Schilte, Pierre Bouzat, Anne Millet, Perrine Boucheix, Karin Pernet-Gallay, Benjamin Lemasson, Emmanuel L. Barbier, Jean François Payen

Research output: Contribution to journalArticlepeer-review

7 Scopus citations


Objectives: Based on evidence supporting a potential relation between posttraumatic brain hypoxia and microcirculatory derangements with cell edema, we investigated the effects of the antiedematous agent mannitol on brain tissue oxygenation in a model of diffuse traumatic brain injury. Design: Experimental study. Setting: Neurosciences and physiology laboratories. Subjects: Adult male Wistar rats. Interventions: Thirty minutes after diffuse traumatic brain injury (impact-acceleration model), rats were IV administered with either a saline solution (traumatic brain injury-saline group) or 20% mannitol (1 g/kg) (traumatic brain injury-mannitol group). Sham-saline and sham-mannitol groups received no insult. Measurements and Main Results: Two series of experiments were conducted 2 hours after traumatic brain injury (or equivalent) to investigate 1) the effect of mannitol on brain edema and oxygenation, using a multiparametric magnetic resonance-based approach (n = 10 rats per group) to measure the apparent diffusion coefficient, tissue oxygen saturation, mean transit time, and blood volume fraction in the cortex and caudoputamen; 2) the effect of mannitol on brain tissue Po2 and on venous oxygen saturation of the superior sagittal sinus (n = 5 rats per group); and 3) the cortical ultrastructural changes after treatment (n = 1 per group, taken from the first experiment). Compared with the sham-saline group, the traumatic brain injury-saline group had significantly lower tissue oxygen saturation, brain tissue Po2, and venous oxygen saturation of the superior sagittal sinus values concomitant with diffuse brain edema. These effects were associated with microcirculatory collapse due to astrocyte swelling. Treatment with mannitol after traumatic brain injury reversed all these effects. In the absence of traumatic brain injury, mannitol had no effect on brain oxygenation. Mean transit time and blood volume fraction were comparable between the four groups of rats. Conclusion: The development of posttraumatic brain edema can limit the oxygen utilization by brain tissue without evidence of brain ischemia. Our findings indicate that an antiedematous agent such as mannitol can improve brain tissue oxygenation, possibly by limiting astrocyte swelling and restoring capillary perfusion.

Original languageEnglish (US)
Pages (from-to)2212-2218
Number of pages7
JournalCritical care medicine
Issue number10
StatePublished - Oct 1 2015


  • Blood oxygenation level dependent
  • Brain edema
  • Brain oxygenation
  • Diffusion-weighted magnetic resonance imaging
  • Magnetic resonance imaging
  • Mannitol
  • Traumatic brain injury

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine


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