Abstract

P 064

High dose methylprednisolone (MP) treatment does not preserve retinal ganglion cells and visual function following ocular ischemia in rats

Dimitriu C., Jehle T., Meschede W., Lasseck J., Bach M., Lagrèze W.
University Eye Hospital Freiburg

Objective: Methylprednisolone (MP) is commonly used to treat traumatic optic neuropathy and optic neuritis. It was neuroprotective in animal models of optic nerve crush but showed negative effects after experimental autoimmune encephalitis. The present study investigated effects of MP on survival of retinal ganglion cells (RGCs) and on retinal and optic nerve function following ocular ischemia.
Methods: Ocular ischemia was induced by increase of intraocular pressure to 120 mmHg for 55 min in adult Brown-Norway rats. Animals were treated either with 15 mg/kg MP or NaCl intraperitoneally direct after and every 12 hours for 3 days. RGCs were labelled retrogradelly 4 days after ischemia and were quantificated 6 days later. Retinal function was evaluated by scotopic and photopic electroretinogram (ERG) 7 days after ischemia. The investigation of the visual pathways by frequency and luminance modulated visual evoked potentials (VEP) was performed on day 4 and 10 after ischemia.
Results: Ocular ischemia lead to a decrease of labelled RGCs to 43±5% (mean±SEM) in the MP group and 47±3% in the NaCl group. ERG did neither differ significantly for scotopic a-wave, b-wave and oscillatory potentials nor for photopic 18 Hz flicker stimulation. 4 days after ischemia VEPs were significantly higher in the MP group 77±9% for temporal and 77±9% for luminance than in the NaCl group: 45±7% and 37±7%, respectively. 10 days later this difference disappeared.
Conclusions: In our experiments high dose treatment with MP did neither improve RGC survival nor retinal function. Delayed decrease of VEP responds indicated only temporal benefit due to steroids. In conclusion, MP treatment neither improved nor impaired ischemic damage of retinal neurons.

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