PROTECTION OF THE TRANSIENTLY ISCHEMIC CAT RETINA BY ZINC-DESFERRIOXAMINE

Purpose. A previous study indicated that hydroxyl radicals are generat ed in the cat retina during the early reperfusion phase after 90 minut es of ischemia. Salicylate was injected intravenously, and its convers ion to 2,3-dihydroxybenzoic acid (2,3-DHBA) served as a marker of hydr oxyl radicals. The authors attempted to prevent this free radical gene ration during reperfusion. Methods. After salicylate administration, b ath eyes (15 minutes apart) of 15 cats were subjected to 90 minutes re tinal ischemia. Following 5 minutes of reperfusion in the control eye, it was enucleated and processed for DHBA quantitation. Then, 7.5 mg o f Zn-desferrioxamine (Zn-DFO) was injected intravenously into nine cat s and saline into six cats. Five minutes later, reperfusion was induce d in the experimental eye for 5 minutes, followed by enucleation. In o ne eye each of 12 other cats, scotopic electroretinographic (ERG) stud ies were carried out during 90 minutes of ischemia and 16 to 18 hours of reperfusion. Five minutes before termination of the ischemia, six a nimals were injected with 7.5 mg Zn-DFO and six with saline. Results. The normalized levels of 2,3-DHBA were lower in the experimental eyes than in their fellow controls only after Zn-DFO treatment (P = 0.01). In the ERG studies, after 16 to 18 hours of reperfusion, the mean b-wa ve-ERG amplitudes in the eyes of the saline-treated cats (n = 6) were 8.4% +/- 4.0% of the preischemic stage, and 70.5% +/- 6.7% of the Zn-D FO-treated cats (n = 6, P = 0.004). Conclusions. Protection of the cat retina against ischemia and reperfusion injury by Zn-DFO was evident, most probably through its inhibitory effect on the generation of hydr oxyl radicals during reperfusion.