Naloxone reduces alterations in evoked potentials and edema in trauma to the rat spinal cord.

The influence of naloxone (an opioid receptor antagonist) on spinal cord conduction and edema formation as a result of trauma to the cord was investigated in a rat model. The spinal cord injury (SCI) was inflicted in urethane anesthetized animals by a longitudinal incision into the right dorsal horn of the T10-11 segments, about 2 mm deep and 5 mm long. Spinal cord evoked potentials (SCEP) were recorded epidurally from the T9 (rostral) and T12 (caudal) segments after stimulation of the ipsilateral tibial and sural nerves at the ankle. The edema was measured by determining water content of the cord at s h after injury. In rats not given naloxone SCI resulted in an immediate long-lasting depression of the rostral maximal negative peak (MNP) amplitude (about 60%) and a significant increase in the latency of the rostral maximal positive peak (MPP). Pretreatment with naloxone inhibited the immediate post-injury decrease of the rostral MNP and some of the increase of MPP latency. The water content in the traumatized spinal cord was reduced by 3% in naloxone treated animals compared with untreated injured controls. Our results indicate that endogenous opioid peptides participate in changes of spinal cord conduction after trauma and influence edema formation probably via multiple opioid receptors.