Long-term ocular effects of osmotic modification of the blood-brain barrier in monkeys. I. Clinical examinations; aqueous ascorbate and protein.

The blood-aqueous humor barrier in adult rhesus monkeys was opened by intracarotid infusion of a 25% mannitol solution. Each monkey had one to four infusions into the same artery, with at least one week between subsequent procedures. The monkeys were observed clinically for 3 to 212 days. Within an hour pigmented cells and protein accumulated in the aqueous humor of the mannitol-treated eyes. Hypotony developed within a day. Aqueous flare and cells cleared within 2 weeks. Hypotony resolved in 8 to 12 weeks. More than one half of the monkeys had transient anisocoria. In some, the pupil in the treated eye was miotic; in others it was dilated. Direct and consensual pupil responses to light remained intact in untreated eyes and in treated eyes with mydriasis. About one fourth of the monkeys developed edema of the ipsilateral optic disk. This correlated with hypotony. No monkey developed cataract, corneal opacity, or vitreous or retinal change. The aqueous protein concentration was slightly above normal a month or more after the carotid infusions, but was considerably less than plasma protein concentration. Posterior and anterior aqueous ascorbate concentrations in treated eyes were slightly below normal, but far greater than plasma concentration, indicating that ascorbate active transport by the ciliary epithelium was essentially intact despite the widespread, permanent structural alteration that had been caused by the mannitol treatment.