Whereas opiate receptor agonists have resulted in spinal cord damage; opiate receptor antagonists have demonstrated protection against spinal cord injury. Because opioids are used in clinical anesthesia, the effect of an opiate antagonist was evaluated on neurologic outcome in a rat model of spinal cord injury occurring during opioid anesthesia. One day prior to spinal cord injury, a catheter was inserted into the spinal subarachnoid space with the tip at T8. On the day of spinal cord injury a balloon tipped catheter was inserted in the epidural space with the tip at the thoracolumbar junction. Spinal cord injury was produced by balloon inflation during one of the following states: 1) group 1 (A/S), injury was produced in awake rats and saline was administered in the subarachnoid space immediately following injury; 2) group 2 (F/S), injury was produced during a fentanyl/nitrous oxide (N2O) anesthetic, and subarachnoid saline administered; and 3) group 3 (F/Nx), injury was produced during a fentanyl/N2O anesthetic, and subarachnoid naloxone (1 mg/kg) was administered immediately following injury. Dose-response curves describing the relationship between the duration of balloon inflation and the percentage of animals with a persistent neurologic deficit were constructed and compared for differences by use of a group t test. The duration of balloon inflation required to produce a neurologic deficit was greater in both the F/S and F/Nx groups than in the A/S group (P < 0.05). There was no difference between the F/S and F/Nx groups. In summary, in rats receiving a fentanyl/N2O anesthetic, neurologic outcome was improved compared with the awake state. The administration of naloxone in the subarachnoid space adjacent to injury did not further improve neurologic outcome. These results do not support the supposition that opioid anesthesia produces an adverse effect upon neurologic outcome following a compressive spinal cord injury.
(C) 1989 American Society of Anesthesiologists, Inc.