BACKGROUND: The pathogenesis of crush syndrome is severe traumatic damageto the organism accompanied by shock and stress, acute toxemia, etc. Glutamate has been shown to be implicatedin excitotoxic neural death in various clinical settings. The high affinity glutamate uptake processplays a key role in normal synaptic transmission. The goal of our research was to determine the levelof glutamate uptake in brain tissue slices after incorporation of [(14)C-U]glutamate. MATERIAL/METHODS:An experimental model of crush syndrome in Wistar male rats was caused by 2 hours of compression of femoralsoft tissues using a special press with a force of 100 kg/1 kg of animal weight. Slices were preparedand glutamate uptake was assayed immediately after compression, and again at 2, 24, and 48 hours of decompression.RESULTS: The level of glutamate uptake in cerebral cortex and hypothalamus slices immediately after compressionwas reduced by 24% (p<0.05) and 31% (p<0.005) respectively. Glutamate uptake in cerebral cortex and hypothalamus was nearly at the same level as the intact group of animals (without compression). In cerebellum slices, glutamate uptake also increased, and in fact exceeded the level in the intact group by 17% (p<0.025). The level of glutamate uptake decreased in cerebral cortex, hypothalamus, and cerebellum slices by 45% (p<0.001), 28% (p<0.001,) and 25% (p<0.001) respectively, compared to the intact group of animals.
Conclusions: Experimental crush syndrome promotes the reduction of the glutamate uptake level in brain tissue slices, such that cerebral cortex > hypothalamus > cerebellum.

Keywords: crush syndrome, Glutamic Acid, in vitro