Purpose - To investigate the role of oxidative injury in ischemic optic neuropathy (ION) and develop an animal model of ION that does not traumatize the eye. Methods - The optic nerve sheath of a patient with a one day history of acute anterior ischemic optic neuropathy was biopsied during optic nerve sheath fenestration (prior to the IONDT results). To detect endogenous hydrogen peroxide the tissue was reacted with cerium chloride and examined by transmission electron microscopy for electron dense hydrogen peroxide derived cerium perhydroxide reaction product. To develop an animal model of ocular ischemia the left internal and external carotid arteries of rats were ligated. The right eyes served as controls. After 30 minutes the ligatures were removed. Animals were sacrificed 1 and 24 hours later. The globes and attached optic nerves were excised and immersed in 1 % 2,3,5-triphenyltetrazolium chloride (TTC) for 30 minutes. The tissue was fixed in 4% paraformaldehyde overnight then processed for cryomicrotomy. Unstained cryosections were examined by light microsopy for the red TTC reaction product. Results - The patient's vision improved from counting fingers to 20/60 immediately following surgery, although the inferior altitudinal defect remained unchanged. Hydrogen peroxide derived reaction product was seen in the meninges of the biopsied optic nerve sheath. In the rat, TTC reaction product was readily visible in the control right eyes and heavily labeled the ganglion cell and inner nuclear layers. In the control right optic nerves, glial cells were also labeled with TTC. In the ischemic left eyes, TTC staining was scant in the retina, predominantly labeling RPE, and it was absent in the optic nerve. Conclusions - (1) The presence of hydrogen peroxide reaction product in the meninges suggests that the optic nerve is exposed to reactive oxygen species during acute ION. (2) The scant TTC staining of ischemic eyes suggests that this model may be used in evaluating the role of free radical scavengers and antioxidants in limiting oxidative injury to the optic nerve during ischemia.
|Journal||Investigative Ophthalmology and Visual Science|
|State||Published - Feb 15 1996|
ASJC Scopus subject areas