Szabo M E, Droy-Lefaix M T, Doly M, Braquet P
Institut Henri Beaufour, Paris, France.
Ophthalmic Res. 1993;25(1):1-9. doi: 10.1159/000267214.
We investigated the contribution of scavenging of oxygen free radicals to retinal ion contents during ischemia and reperfusion with the use of superoxide dismutase (SOD, Sigma), allopurinol (Sigma), EGB 761 (extract of Ginkgo biloba, Tanakan, IPSEN, Paris, France) and allopurinol plus EGB 761 in the rat. SOD (15,000 U/kg/day), allopurinol (50 mg/kg/day), EGB 761 (100 mg/kg/day) and allopurinol (50 mg/kg/day) plus EGB 761 (100 mg/kg/day) were administered for 10 days, respectively. Then, the eyes were subjected to 90 min of ischemia followed by 4 and 24 h of reperfusion, respectively. Retinal Na+, K+, Ca2+ and Mg2+ contents were measured by atomic absorption spectrophotometry after the washing out of blood and extracellular fluid from the vasculature. SOD, EGB 761 and the combination of EGB 761 with allopurinol significantly reduced the ischemia/reperfusion-induced Na+ and Ca2+ accumulation and K+ loss in ischemic/reperfused retinal tissue. Allopurinol alone failed to reduce the maldistribution of Na+, Ca2+ and K+ induced by ischemia/reperfusion in the retina. Neither intervention inhibited the cell Mg2+ loss which was observed during ischemia and reperfusion. Despite the responsible mechanisms remaining controversial, many studies confirmed that ischemia/reperfusion could trigger very sudden metabolic, electrophysiologic, morphologic and functional changes. There is general agreement that major ionic shifts are implicated; what triggers these changes is unclear, although many investigators believe that free radicals and oxidant stress may be important.(ABSTRACT TRUNCATED AT 250 WORDS)
