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.

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Differential responses to induced changes in systemic blood pressure (BP) at different layers of both the retinal and choroidal vasculature were observed, by monitoring localized PO2 as a function of depth, in the retina and choroid of the rat eye using oxygen-sensitive recessed microelectrodes. Visual and electrophysiological localization of the microelectrode tip allowed the oxygen distribution to be related to the positions of the vascular beds of the retina and choroid. Highly reproducible intraretinal PO2 profiles were achieved. The relationship between PO2 and systemic BP was linear in the deep capillary layer of the retina (PO2 = 0.17 x BP - 2.63) and in the choriocapillaris (PO2 = 0.21 x BP + 2.95), whereas it was nonlinear in the superficial retinal capillary layer [PO2 = 40.01/[1 + (BP/66.22)-1.22]] and deep choroid [PO2 = 83.82/[1 + (BP/124.61)-0.87]]. The minimum PO2 occurred between the two retinal capillary beds, and a PO2 gradient was evident in the choroid. The contrasting responses of different layers of the two circulations reflect different blood flow control mechanisms not evident when studying the circulations as a whole.

Occlusion of the retinal circulation renders most of the inner retina anoxic. Ventilation with 100% oxygen does not generally avoid some degree of intraretinal anoxia. With 100% oxygen ventilation, the oxygen consumption of the inner retina was more than four times that of the outer retina. A marked degree of heterogeneity in oxygen uptake of different retinal layers was evident. The dominant oxygen consumers were the inner segments of the photoreceptors, the outer plexiform layer, and the inner plexiform layer.

1. The present review reports some of the earliest physiological changes that occur in the diabetic retina prior to any clinical or anatomical changes in an animal model of diabetes. 2. Using chemically induced diabetes (by streptozotocin) in rats, retinal blood flow and vitreal and retinal oxygen tension were determined after 5 weeks of sustained hyperglycaemia. Blood flow was greater and was also redistributed in the diabetic group compared with values for the control group. At the same time, oxygen tension distribution was altered around retinal arterioles, implying an increase in retinal oxygen consumption in these early diabetic retinas. 3. The possibility that the blood flow changes could be due to altered control mechanisms in the retinal vasculature was confirmed using an isolated, perfused eye preparation. In diabetic eyes an altered reactivity to test pharmacological agents was demonstrated after 4 weeks of diabetes. 4. To further explore these vascular response changes we developed an isolated, perfused retinal arteriolar preparation in which individual segments of the vasculature can be tested. The possibility that insulin has a direct vasodilator effect on retinal arterioles was confirmed and was demonstrated to act via nitric oxide released from the vascular endothelial cells. These data may implicate the diabetic-induced insulin changes in early retinal changes. 5. Evidence is presented that although early glucose control may be vital in stopping the onset of diabetic retinopathy, there comes a stage in the induced diabetic cascade where if the retinopathy has commenced, good glucose control cannot stop the further progression of the retinopathy.