Microvascular perfusion and metabolism in injured spinal cord after methylprednisolone treatment

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Abstract
The effect of treatment with the synthetic glucocorticoid methylprednisolone on the microvasculature and metabolism of the traumatized spinal cord was studied. Spinal cords of cats were compressed with a 170-g weight for 5 min and were treated with either high-dose methylprednisolone (HDMP, 15 mg/kg per 24 h) or megadose methylprednisolone (MDMP, 60 mg/kg per 24 h). Animals were sacrificed at 2, 8 or 24 h following injury. Treatment with HDMP resulted in substantial preservation of injured spinal cord microvascular perfusion at 8 h compared with injured untreated cats. Compression trauma caused a partial derangement of energy metabolism and a shift toward anaerobic glycolysis in both treated and untreated groups for the entire 24-h postinjury period. Tissue levels of ATP, phosphocreatine and total adenylates in the HDMP-treated cats sacrificed at 8 h ater trauma were significantly elevated over untreated controls, but those in the 2 and 24 h groups were not. Concentrations of energy intermediates in MDMP-treated cats were either equal to or below those of injured untreated animals at all 3 post-injury time periods. The postinjury metabolite pattern and concentrations possibly result from differing levels of blood flow and neuronal activity in the injured untreated, HDMP, and MDMP-treated spinal cords. Better tissue perfusion in the HDMP-treated cats might be expected to result in an improved tissue energy state in these aimals. Intensive high-dose glucocorticoid treatment augmented spinal cord monosynaptic and polysynaptic reflex transmission and primary afferent excitability. Acute single i.v. dose studies show this direct neuronal action to be dose-related. Additional high-energy phosphate molecules that may be reformed as a result of HDMP treatment were perhaps used as the energy source for any increased neuronal activity caused by steroid administration. Beneficial effects of glucocorticoid treatment in experimental spinal cord trauma might derive from preserved cellular structural integrity. This could resut in increased levels of neuronal activity, energy utilization and production in treated compared with untreated tissue.