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From the *Department of Surgical and Radiological Sciences, Veterinary Medical Teaching Hospital, University of California at Davis, Davis, California;
Klinik für Anaesthesiologie; and
Department for Medical Statistics and Epidemiology, Klinikum rechts der Isar, Technische Universität München, Munich, Germany;
Klinik für Anästhesiologie, Klinikum der Johannes Gutenberg-Universität, Mainz, Germany.
Address correspondence and reprint requests to Eva Eberspächer, DVM, University of California, Veterinary Medical Teaching Hospital, Anesthesia/Critical Patient Care, One Shields Ave., Davis, CA. Address e-mail to eberspaecher{at}ucdavis.edu.
BACKGROUND: Propofol 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).
METHODS: Animals 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.
RESULTS: Lesion 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.
CONCLUSION: Despite 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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