Retinal vascular architecture is maintained in retinal degeneration: corrosion cast and electron microscope study

Purpose To demonstrate the changes of the retinal vascular architecture in the diffusely degenerated thin retina. Methods Three-week-old weanling Wistar Kyoto rats were divided randomly int o two groups. One group (n = 20) was fed a vitamin E-deficient solid diet a nd the other group (n = 20) was fed a solid rat chow diet. Rats were mainta ined on their respective diets for 14 months and then killed for scanning e lectron microscopy of vascular corrosion casts, light and electron microsco py and biochemical determinations. Results The serum level of vitamin E in the E-deficient rats was 1.0 mu0.49 mug/ml, while that in the rats fed a normal diet was 13.7 +/-1.0 mug/ml (S tudent's t-test, p = 0.0001). In vitamin E-deficient rats, light microscopy showed degenerated retinas only half as thick as normal. Corrosion casts a nd scanning electron microscopy revealed that the retinal capillaries of th e entire retina were decreased in number and scattered with localised narro wing, calibre irregularity and frequent loop formation. In the posterior po le of the retina, some capillaries clustered into small tortuous knots. How ever, the two-layered architecture of the capillary network in the retina w as maintained. The differences in calibre of retinal capillaries between th e vitamin E-deficient and normal rats were statistically significant (p < 0 .0001). No remarkable abnormal changes were observed in the large retinal v essels other than arterial calibre differences (p < 0.022). No arteriovenou s shunts, crossing defects or microaneurysms were seen. Transmission electr on microscopy revealed complete disappearance of the photoreceptor outer an d inner segments and nuclei. The retinal pigment epithelium contained lipof uscin granules and retinal capillaries with narrow lumens. The capillary en dothelial cells were thickened and had scarce cytoplasmic components with v acuoles and irregularly thickened basement membranes. The capillary pericyt es had vacuoles. No abnormalities were seen in the control normal rats. Conclusion These findings indicate that the decrease in retinal capillaries in vitamin E-deficient rats is secondary to retinal degeneration. It was a ssumed that the morphological changes in the capillary network reflected st ructural damage to the retinal vascular cells caused by free radicals, and lipid peroxides generated by oxidation. However, even in such severe degene ration the retinal vascular architecture, including the main artery and vei n and two-layer capillary networks, was maintained. This is may be because of the basic anatomical arrangement of the blood vessels.