Nayak M S, Kita M, Marmor M F
Department of Ophthalmology, Stanford University School of Medicine, CA 94305-5308.
Invest Ophthalmol Vis Sci. 1993 May;34(6):2018-22.
To provide evidence that free radical damage is a component of postischemic retinal injury; to determine whether antioxidant enzymes, superoxide dismutase (SOD) and catalase, can protect the retina from ischemic injury.
Total retinal ischemia for 60 or 75 min was produced in Dutch rabbits by raising intraocular pressure. Retinal recovery was monitored with the electroretinogram. Enzymes were administered as an intravenous bolus dose 2-3 min before restoration of circulation.
In eyes subjected to 60 min ischemia, the amplitude of the a-wave 4 hours after reperfusion averaged 114.9% of baseline value in control rabbits and 126.5% in SOD-treated animals. The b-wave amplitude at this time was 79.3% and 106.8% in control rabbits and SOD-treated rabbits, respectively. After an ischemic insult of 75 min, at 4 hours the a-wave amplitude was 89.2% of baseline in control eyes, 108.8% in SOD-treated eyes, 159.6% in eyes that received a combination of SOD and catalase, and 149.8% in catalase-treated eyes. The amplitude of the b-wave was reduced to 47.8% in control eyes and 44.8% in SOD-treated eyes, but recovered to 92.3% in rabbits that received the combination therapy and 98.8% in animals that received catalase alone.
These findings suggest that free radical generation is involved in ischemic tissue damage. The fact that antioxidant enzymes can be protective has implications for the treatment of acute ischemic diseases of the retina.
