BREAKDOWN OF BLOOD - RETINAL BARRIER IN RCS RATS WITH INHERITED RETINAL DEGENERATION

  • 1 January 1980
    • journal article
    • research article
    • Vol. 43  (5) , 418-426
Abstract
A breakdown in the blood-retinal barrier to certain proteins is described in mutant RCS [Royal College of Surgeons] rats with inherited retinal degeneration. Microperoxidase and horseradish peroxidase injected i.v. were extravasated from the outer (but not inner) retinal capillaries of these rats at approximately 11 wk old or older. The number of affected capillaries increased with the age of the animals and progression of the retinal dystrophy until virtually all capillaries in the outer retina were permeable to these tracers. In these capillaries, enzyme reaction product were found in a greater proportion of luminal vesicles and in the majority of abluminal vesicles. Reaction product was localized in cytoplasmic vacuoles, the basal laminae of endothelial cells and pericytes, and the perivascular spaces. The increased permeability of outer retinal capillaries in RCS rats appeared due to an increase in transendothelial vesicular transport of the probe molecules. The tracers did not appear to permeate the interendothelial junctions or enter the basal laminae by reflux from the perivascular spaces. Factors originating from the degenerated photoreceptor cells may play a role in stimulating the vesicular transport in permeable capillaries. The outer retinal capillaries of RCS rats were not permeable to Hb, catalase or ferritin, regardless of the age of the animal or the degree of retinal degeneration. Since the vesicles that form at the luminal front are covered by a diaphragm, this structure may prevent entry of these larger proteins into the endothelial vesicle, even in capillaries permeable to the smaller tracers.

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