Fig. 4. Breakdown in the posterior blood ocular barrier resulting from poisoning by various doses of sodium iodate and demonstrated by the diffusion of intravenously injected horseradish peroxidase through the whole thickness of the retina via the damaged RPE (experiments carried out in rabbit by McKechnie and Foulds (unpublished)). a & c, control tissue b & d, effects of intravenous sodium iodate. which, if allowed to accumulate, would lead to retinal separation.(See Steinberg for review). 7

Ionic movement across the RPE apical and basal membranes is reflected in the standing potential of the eye and the'c'wave of the ERG, both of which can be increased in amplitude by the administration of substances which stimulate ionic transfer such as sodium azide, 8, 9 or reduced or even abolished by poisons which selectively inhibit RPE func tion, notably sodium iodate as demonstrated many years ago by Noell. 10 Not unexpectedly, poisoning of the RPE by sodium iodate leads to severe metabolic upset and structural change in the related outer ret ina and to a breakdown in the posterior blood ocular barrier as demonstrated by the use of