ROLE OF REACTIVE OXYGEN SPECIES IN OPTIC-NERVE COMPRESSION INJURY - APRELIMINARY-STUDY

Optic nerve compression is one of the complications in craniofacial su rgery and blepharoplasty. We have shown previously that acute and chro nic nerve compression produce significant tissue injury in rat sciatic nerve. In the present study the optic nerve was evaluated for possibl e ischemia/reperfusion injury after acute compression in an animal mod el. Male New Zealand White rabbits were used in the experiment. The op tic nerve was subjected to 2-hour compression followed by reperfusion for 1 hour. Nerve compression was established by banding the optic ner ve with silastic tubing. The compressed optic nerve was assayed for ma londialdehyde, an indicator of lipid peroxidation, measured as thiobar bituric acid reactive substances (TEARS). The TEARS levels increased s ignificantly to 2.5 times normal, from 37 +/- 6 pmoles per milligram t issue (N = 6) to 90 +/- 12 pmoles per milligram tissue dry weight (N = 5) in the compressed/reperfused nerve (p < 0.05). Much of these incre ases were prevented by treatment with deferoxamine, an iron chelator a nd antioxidant. The results indicate that optic nerve is injured by ac ute compression followed by reperfusion. The nerve compression injury appears to be due to reactive oxygen species and can he ameliorated by treatment with free radical scavengers.