Acute experimental allergic encephalomyelitis increases lumbar spinal cord incorporation of epidurally administered [³H]-D-mannitol and [¹⁴C]-carboxyl-inulin in rabbits

We sought to determine whether acute experimental allergic encephalomyelitis (EAE) alters the incorporation of epidurally administered [³H]-D-mannitol and [¹⁴C]-carboxyl-inulin into the lumbar spinal cord in rabbits. Acute EAE is an experimental model for demyelinating spinal cord diseases such as multiple sclerosis. It was induced in rabbits by footpad inoculation with rabbit spinal cord homogenate, resulting in hind limb paresis or paralysis. Animals were classified into four study groups: Control, Paraparesis, 1-Day Paraplegia, and 5-Day Paraplegia. Ten μCi each of [³H]-D-mannitol and [¹⁴C]-carboxyl-inulin were administered epidurally for 90 min. After infusion, animals were perfused with saline. The lumbar cord was dissected and divided into 11 segments. Compared with other groups, animals in the 5-Day Paraplegia group had greater incorporation of [³H]-D-mannitol and [¹⁴C]-carboxyl-inulin in lumbar segment 8, corresponding to the location of the epidural catheter tip. Compared with the Control group, EAE animals had increased [³H]-D-mannitol incorporation in various lumbar segments. Increases in the spinal cord incorporation of epidural drugs with EAE suggest that demyelination may render the spinal cord susceptible to larger amounts of substances administered in the epidural space. These findings may have implications regarding neurotoxicity in association with demyelinating spinal cord disease.