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Uric acid as biochemical marker for retinal and optic nerve damage after occlusion and reperfusion of common carotid and vertebral arteries in rat.

Transient retinal and optic nerve ischemia lasting for 20 minutes was produced in Wistar rats by clipping bilateral common carotid arteries and coagulating both vertebral arteries by heat. The uric acid level in the retina and optic nerve were determined by high performance liquid chromatography with electrochemical detection just before induction of ischemia, 20 minutes after induction of ischemia, and after resolution of ischemia. Uric acid content in the optic nerve (28.0 +/- 4.5 ng/mg protein) was about 5 times higher than that in the retina (5.7 +/- 0.8 ng/mg protein) in the control experiment. Ischemia lasting for 20 minutes caused a 2.7-fold increase of uric acid in the optic nerve and a 1.8-fold increase in the retina. Following reperfusion of the blood flow by unclipping of the common carotid arteries, the uric acid level decreased to the control level in both the retina and optic nerve 30 minutes after unclipping, which was followed by 3.1- and 1.6-fold increases in uric acid in the retina and the optic nerve, respectively, at 60 minutes after unclipping. Although ischemia alone causes tissue damage, there is some clinical evidence that greater injury can occur after oxygen is reintroduced to ischemic tissue. Our results indicate that the retina is more likely to be damaged by reperfusion than the optic nerve.