Role of reactive oxygen species in optic nerve compression injury: a preliminary study

Optic nerve compression is one of the complications in craniofacial surgery and blepharoplasty. We have shown previously that acute and chronic nerve compression produce significant tissue injury in rat sciatic nerve. In the present study the optic nerve was evaluated for possible ischemia/reperfusion injury after acute compression in an animal model. Male New Zealand White rabbits were used in the experiment. The optic nerve was subjected to 2-hour compression followed by reperfusion for 1 hour. Nerve compression was established by banding the optic nerve with silastic tubing. The compressed optic nerve was assayed for malondialdehyde, an indicator of lipid peroxidation, measured as thiobarbituric acid reactive substances (TBARS). The TBARS levels increased significantly to 2.5 times normal, from 37+/-6 pmoles per milligram tissue (N=6) to 90+/-12 pmoles per milligram tissue dry weight (N=5) in the compressed/reperfused nerve (p < 0.05). Much of these increases were prevented by treatment with deferoxamine, an iron chelator and antioxidant. The results indicate that optic nerve is injured by acute compression followed by reperfusion. The nerve compression injury appears to be due to reactive oxygen species and can be ameliorated by treatment with free radical scavengers.