Spinal cord energy metabolism following compression trauma to the feline spinal cord

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Abstract
The spinal cord metabolic state was determined for 24 h after compression trauma to the feline spinal cord. Cats were anesthetized with pentobarbital and injured by placing a 190 g weight on the spinal cord for 5 min. Biochemical analysis of the injured segment revealed a significant depletion in the levels of ATP, phosphocreatine (P-creatine) and total adenylates for the entire 24 h recovery period. Glucose levels initially declined but by 1 h had normalized and at 8 and 24 h were significantly supranormal. The lactate-pyruvate ratio and tissue lactate concentrations increased 4 and 5 1/2 times, respectively, for the first 4 h after injury. Between 8-24 h, lactate levels remained elevated, the lactate-pyruvate ratio declined to control levels as the result of a significant rise in the tissue pyruvate concentration. Metabolism was probably not homogeneous throughout the injured segment and the tissue metabolic rate was depressed for the initial 4 h after trauma, then increased in metabolically active tissue for the remainder of the 24 h recovery period. This model of spinal cord trauma results in a severe, prolonged ischemia and metabolic injury to the affected tissue. Whether these metabolic changes result from or cause the tissue damage and irreversible paraplegia associated with this type of spinal cord injury remains to be determined.