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

Abstract

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 into two groups. One group (n = 20) was fed a vitamin E-deficient solid diet and the other group (n = 20) was fed a solid rat chow diet. Rats were maintained on their respective diets for 14 months and then killed for scanning electron microscopy of vascular corrosion casts, light and electron microscopy and biochemical determinations.

Results: The serum level of vitamin E in the E-deficient rats was 1.0 +/- 0.49 microg/ml, while that in the rats fed a normal diet was 13.7 +/- 1.0 microg/ml (Student's t-test, p = 0.0001). In vitamin E-deficient rats, light microscopy showed degenerated retinas only half as thick as normal. Corrosion casts and scanning electron microscopy revealed that the retinal capillaries of the entire retina were decreased in number and scattered with localised narrowing, calibre irregularity and frequent loop formation. In the posterior pole of the retina, some capillaries clustered into small tortuous knots. However, the two-layered architecture of the capillary network in the retina was maintained. The differences in calibre of retinal capillaries between the vitamin E-deficient and normal rats were statistically significant (p < 0.0001). No remarkable abnormal changes were observed in the large retinal vessels other than arterial calibre differences (p < 0.022). No arteriovenous shunts, crossing defects or microaneurysms were seen. Transmission electron microscopy revealed complete disappearance of the photoreceptor outer and inner segments and nuclei. The retinal pigment epithelium contained lipofuscin granules and retinal capillaries with narrow lumens. The capillary endothelial cells were thickened and had scarce cytoplasmic components with vacuoles and irregularly thickened basement membranes. The capillary pericytes 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 assumed that the morphological changes in the capillary network reflected structural damage to the retinal vascular cells caused by free radicals and lipid peroxides generated by oxidation. However, even in such severe degeneration the retinal vascular architecture, including the main artery and vein and two-layer capillary networks, was maintained. This is may be because of the basic anatomical arrangement of the blood vessels.