Intraretinal oxygen distribution in the monkey retina and the response to systemic hyperoxia.

Purpose: To measure the intraretinal oxygen distribution and consumption in the fovea, the parafovea, and the inferior retina in the monkey eye and determine the influence of graded systemic hyperoxia.
Methods: Oxygen sensitive microelectrodes were used to measure the oxygen tension as a function of depth through the retina in anesthetized monkeys (n = 8) under normoxic and hyperoxic conditions. Oxygen consumption rates in the avascular regions of retina were determined by fitting the oxygen profiles to established oxygen consumption models.
Results: Under normoxic conditions, in the foveal area, the intraretinal oxygen distribution reflected the absence of retinal capillaries and the predominantly choroidal origin of retinal oxygenation. A similar shape of oxygen distribution was seen in the parafoveal retina with the addition of local perturbations in the inner retina attributed to the presence of retinal capillaries. In the inferior retina the same general shape was found. Oxygen consumption in the outer retina was higher in the parafoveal region, and the minimum oxygen tension was lower. During hyperoxia, choroidal oxygen levels in all areas increased dramatically, but the increase in oxygen tension in the inner retina was much less. The avascular nature of the foveal area allowed oxygen consumption analysis of both the inner and outer retina and showed that inner retinal oxygen consumption increased significantly during hyperoxic ventilation to a level equivalent to that of the outer retina.
Conclusions: In the outer retina of the monkey the P(O2) minimum is lower, and the oxygen consumption rate is higher in the parafoveal region. During systemic hyperoxia, outer retinal oxygen consumption is unaffected, but in the foveal area, total oxygen consumption increases. This regulation of oxygen consumption in the monkey retina is comparable to that reported in lower mammals and may represent an important mechanism in retinal homeostasis.