Time course of energy perturbation after compression trauma to the spinal cord: an experimental study in the rat using microdialysis.

Changes occurring in the extracellular fluid (ECF) concentration of energy-related metabolites were investigated in a well-characterized model of compression trauma to the spinal cord. Microdialysis probes were inserted into exposed grey matter of the dorsal horn at the level of Th 7-8, and perfused with mock cerebrospinal fluid. The trauma was produced 2 hours later by compression of the cord with a 9-, 35-, or 50-g load for 5 min. Microdialysis samples (10-minute fractions) were collected for another 2 hours following decompression. The trauma was associated with an accumulation of lactate, inosine, and hypoxanthine, and an increase in the lactate/pyruvate ratio in the ECF, indicating a profound disturbance in energy metabolism. These changes were related to the severity of spinal cord injury as well as to the spinal cord blood flow (SCBF) reductions and neurological deteriorations previously determined. Following decompression, all ECF metabolites normalized within 20-40 min after mild (9 g) to moderate (35 g) trauma. After severe trauma (50 g), resulting in complete ischemia during compression, followed by irreversible paraplegia, there was a partial recovery of ECF inosine and hypoxanthine, whereas the increase in lactate and the lactate/pyruvate ratio persisted. The results suggest that penumbra conditions prevail during the early posttraumatic period when the degree of trauma results in severe neurological deterioration and that ECF lactate levels in the spinal cord is a sensitive indicator of secondary ischemia after compression injury.