The increase of retinal vessel oxygen saturation in diabetic retinopathy points to a diabetic microvascular alteration. This may be due to occlusions and obliterations in the capillary bead and the formation of arterio-venous shunt vessels. On the other hand, hyperglycaemia-induced endothelial dysfunction, with subsequent suppression of the endothelial NO-synthase and disturbance of the vascular auto-regulation, may contribute to retinal tissue hypoxia.
A new method for the spatially resolved measurement of the oxygen saturation of retinal vessels is described. Imaging spectrometry was used for both measurements of transmission and reflectance spectra of whole blood in cuvettes as well as for fundus reflectance spectra. A model was developed for the calculation of the oxygen saturation, valid in the wavelength range between 510 nm and 586 nm, in that the internal reflectance is constant and only the transmitted light depends on layer thickness and hematocrit. Altogether 265 measurements were performed in different number at 30 eyes. In each measurement, the oxygen saturation was simultaneously determined for 193 locations along a line of 1.5 mm at the fundus. The mean oxygen saturation in retinal arteries was (92.2 +/- 4.1)% and (57.9 +/- 9.9)% in retinal veins. The mean retinal arterio-venous difference of the oxygen saturation was (35.1 +/- 9.5)%. The venous oxygen saturation depended on distance from the optic disc. The measured mean of the arterio-venous difference of the oxygen saturation corresponded well to the value of the brain (34%). The utilization of oxygen in the temporal quadrants (inferior: 39.4 +/- 10.4%) is significantly (p = 0.05) higher than in the nasal quadrants (inferior: 31.3 +/- 6.7%).
Noninvasive measurement and quantitative analysis of the Bayliss effect in human retinal vessels by means of the RVA is possible. Analysis of retinal arterial autoregulation may provide valuable insight into pathologic conditions such as diabetic or hypertensive retinopathy.
The supplementation of L, Z, O-3-LCPUFAs and antioxidants resulted in considerable increase in MPOD. There was no difference in accumulation of MPOD between both dosages. Thus, we believe that the used supplementation with L and Z seems to reach a saturation level in retinal cell structure. Additionally, the constant supplementation of L, Z, O-3-LCPUFAs and antioxidants in AMD patients seems to be useful, because MPOD reduces without supplementation. We conclude that the supplementation caused an increase of MPOD, which results in an improvement and stabilization in BCVA in AMD patients. Thus, a protective effect on the macula in AMD patients is assumed.
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