SPINAL-CORD EVOKED-POTENTIALS AND EDEMA IN THE PATHOPHYSIOLOGY OF RATSPINAL-CORD INJURY - INVOLVEMENT OF NITRIC-OXIDE

The possibility that nitric oxide is somehow involved in the early bio electrical disturbances following spinal cord injury in relation to th e later pathophysiology of the spinal cord was examined in a rat model of spinal cord trauma. A focal trauma to the rat spinal cord was prod uced by an incision of the right dorsal horn of the T 10-11 segments u nder urethane anaesthesia. The spinal cord evoked potentials (SCEP) we re recorded using epidural electrodes placed over the T9 and T12 segme nts of the cord following supramaximal stimulation of the right tibial and sural nerves in the hind leg. Trauma to the spinal cord significa ntly attenuated the SCEP amplitude (about 60%) immediately after injur y which persisted up to 1h. However, a significant increase in SCEP la tency was seen at the end of 5h after trauma. These spinal cord segmen ts exhibited profound upregulation of neuronal nitric oxide synthase ( NOS) immunoreactivity, and the development of edema and cell injury. P retreatment with a serotonin synthesis inhibitor drug p-chlorophenylal anine (p-CPA) or an anxiolytic drug diazepam significantly attenuated the decrease in SCEP amplitude, upregulation of NOS, edema and cell in jury. On the other hand, no significant reduction in SCEP amplitude, N OS immunolabelling, edema or cell changes were seen after injury in ra ts pretreated with L-NAME. These observations suggest that nitric oxid e is somehow involved in the early disturbances of SCEP and contribute to the later pathophysiology of spinal cord injury.