Pharmacological Transection of Brain-Spinal Cord Communication Blocks Pain-Induced Hemorrhage and Locomotor Deficits after Spinal Cord Injury in Rats.
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abstract
Spinal cord injury (SCI) is often accompanied by additional tissue damage (polytrauma), which engages pain (nociceptive) fibers. Prior research has shown that nociceptive input can increase cell death, expand the area of hemorrhage, and impair long-term recovery. The current study shows that these adverse effects can be blocked by the sodium channel blocker lidocaine applied rostral to a contusion injury. Rats received a lower thoracic (T12) contusion injury, and noxious electrical stimulation (shock) was applied to the tail 24h later. Immediately before shock treatment, a pharmacological transection was performed by slowly infusing lidocaine at T2. Long-term locomotor recovery was assessed over the next 21 days. Noxious electrical stimulation impaired locomotor recovery, and this effect was blocked by rostral lidocaine. Next, the acute effect of lidocaine was assessed. Tissue was collected 3h after noxious stimulation, and the extent of hemorrhage was evaluated by assessing hemoglobin content using Western blotting. Nociceptive stimulation increased the extent of hemorrhage. Lidocaine applied at T2 before, but not immediately after, stimulation blocked this effect. A similar pattern of results was observed when lidocaine was applied at the site of injury by means of a lumbar puncture. The results show that a pharmacological transection blocks nociception-induced hemorrhage and exacerbation of locomotor deficits.
