RESUMO
A cortical tissue necrosis from focal trauma expands to 150% of its initial volume within 24 hrs. It is currently unknown, whether this phenomenon is part of the primary traumatic lesion or if it involves secondary mechanisms such as the release of excitatory amino acids into the traumatic penumbra zone. A microdialysis probe was inserted for that purpose in an oblique angle into the cortex of Sprague-Dawley rats, approximately 2 mm below the brain surface. One day later a highly standardized cortical freezing lesion was induced at the brain cortex above the microdialysis probe. Dialysate was collected prior to, during, and after trauma in 10 min intervals. In each animal, it was confirmed histologically, that the tip of the microdialysis probe was localized in the grey matter in close vicinity to the primary lesion. Following induction of the trauma a statistically significant increase of the dialysate level of aspartate, glutamate, glycine, and serine was observed, whereas that of alanine was not altered throughout the experiment. The posttraumatic increase of the excitatory neurotransmitters aspartate and glutamate indicates that these amino acids are involved in the secondary lesion growth after trauma. Confirmation of this hypothesis would require that specific antagonization of these excitotoxic amino acids is inhibiting growth of the lesion.
