• Eva Eberspächer, Kerstin Heimann, Regina Hollweck, Christian Werner, Gerhard Schneider, and Kristin Engelhard.
• Department of Surgical and Radiological Sciences, Veterinary Medical Teaching Hospital, University of California at Davis, One Shields Ave., Davis, CA, USA. eberspaecher@ucdavis.edu
• Anesth. Analg. 2006 Dec 1;103(6):1527-33.

BackgroundPropofol is commonly used to sedate patients after traumatic brain injury. However, the dose-dependent neuroprotective effects of propofol after head trauma are unknown. We compared histopathological damage after 6 h of electroencephalogram-targeted high- and low-dose propofol infusion in rats subjected to controlled cortical impact (CCI).MethodsAnimals were randomly assigned to CCI/propofol with electroencephalogram burst-suppression-ratio 1%-5% (CCI/lowprop), CCI/propofol with burst-suppression-ratio 30%-40% (CCI/highprop), control group CCI/1.0 vol % halothane (CCI/halo), or sham group with halothane anesthesia (SHAM/halo). Brain slices were stained with kresyl violet (KV) and hematoxylin/eosin (HE) to evaluate lesion volume, number of eosinophilic cells, and activation of caspase-3 in the hippocampus.ResultsLesion volume (mm3) and number of eosinophilic cells in the hippocampus did not differ significantly [lesion volumes: CCI/lowprop 31.55 +/- 14.66 (KV) and 53.77 +/- 8.62 (HE); CCI/highprop 33.81 +/- 10.57 (KV) and 52.30 +/- 11.55 (HE); CCI/halo 36.42 +/- 17.06 (KV) and 57.95 +/- 8.49 (HE)]. Activation of caspase-3 occurred in the ipsilateral hippocampus in all CCI-groups.ConclusionDespite different levels of cortical neuronal function, there were no relevant differences in the short-term histopathological damage. These results challenge the view that the neuroprotective effect of propofol relates to the suppression of cerebral metabolic demand.

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