EFFECTS OF NALOXONE ON SODIUM-ACTIVATED AND POTASSIUM-ACTIVATED AND MAGNESIUM-DEPENDENT ADENOSINE-5'-TRIPHOSPHATASE ACTIVITY AND LIPID-PEROXIDATION AND EARLY ULTRASTRUCTURAL FINDINGS AFTER EXPERIMENTAL SPINAL-CORD INJURY

ENDORPHINS HAVE BEEN implicated in the pathophysiology of spinal cord injury. The effect of naloxone on the sodium- and potassium-activated and magnesium-dependent adenosine-5'-triphosphatase (Na+-K+/Mg+2 ATPas e, EC.3.6.1.3.) activity, lipid peroxidation, and early ultrastructura l findings were studied in rats at the early stage of spinal cord inju ry, produced with an aneurysm clip on the T2-T7 segments. The rats wer e divided into four groups, The 10 rats in Group I, which had no injur y and received no medication, were used for determining Na+-K+/Mg+2 AT Pase activity, the extent of lipid peroxidation (by measuring the leve l of thiobarbituric acid-reactive substances as malondialdehyde), and normal ultrastructural findings. On the 15 rats in Group II, without s pinal cord injury, only laminectomy was performed to determine the eff ect of surgery on the biochemical indices and findings. In the 15 rats in Group III, physiological saline was administered intraperitoneally in an amount equivalent to that of the naloxone administered immediat ely after spinal cord injury. In the 15 rats in Group IV, 0.5 mg of na loxone was administered intraperitoneally as a single dose immediately after injury and again 60 minutes after injury. The Na+-K+/Mg+2 ATPas e activity was promptly reduced after spinal cord injury and remained in a lower level than the levels of Groups I and II during 120 minutes after injury. Naloxone treatment, immediately after trauma, attenuate d the inactivation of Na+-K+/Mg+2 ATPase. On the other hand, there was a significant difference in the malondialdehyde content between anima ls in Groups I and III. Naloxone treatment reduced the malondialdehyde content in Group IV. These data suggest the possibility that naloxone contributes to protecting the spinal cord from injury by effecting li pid peroxidation and cell membrane stabilization. The possible effect mechanism of naloxone, which attenuates the inactivation of Na+-K+/Mg2 ATPase and decreases lipid peroxidation, is discussed.