[Excitatory amino acids and prostanoids release in spinal cord injury]

Acute spinal cord trauma may initiate a cascade of hemodynamic and biochemical events characterized by direct mechanical destruction of neurons, hemorrhages and significant increases in active substances (glutamate, prostaglandins (PGs), ets.). However, there are no data which define the effect of acute spinal cord trauma on biochemical changes in the spinal cord. The aim of the present study was to examine time-dependent biochemical changes in the spinal cord by intrathecal microdialysis in the acute stage of spinal cord turama.

Male Sprague-Dawley rats (300-325g) were implanted with a dialysis catheter and PE-10 catheter in the intrathecal space of the lumbar spinal cord. Three days later the animals were anesthetized with halothane and 10-min dialysis samples were collected. Compression spinal cord injury was produced by inflating an extradural 2F-Fogarty balloon catheter (L4-L5) for 60 sec. After compression, samples were collected while the animals remained anesthetized for 30 min, and additional samples were collected until 4hr post-injury. At the end of the dialysis period neurological function was briefly evaluated. Microdialysate samples were analyzed for glutamate, aspartate, and taurine by HPLC-UV and for PGE2 by RIA.

Compression of the spinal cord caused significant increases in the levels of all amino acids. The greatest in creases were in glutamate and aspartate at 10 min, followed by a decrease over the rest of the 4-hr period. Similarly, PGE2 showed an immediate increase after compression, with normalization between 1-2 hr, but this was followed by a secondary increase at 2-4 hr. Neurologically, all animals displayed complete paralysis with loss of sensory function that remained unchanged for the 4-hr period.

The present study clearly demonstrated the time course of spinal amino acids and PGE2 release by using a chronically implanted dialysis catheter after spinal cord compression and also showed a correlation with neurological deterioration. These biochemical changes in the extracellular space may display various, multiphasic patterns reflecting progressively developing edema and corresponding ischemia.