Intraocular pressure and aqueous humor formation rate have been determined from the first trimester of pregnancy through term, with further determinations 3 months postpartum, in 7 patients. The intraocular pressure showed a consistent, statistically significant fall during pregnancy, returning to values seen in early pregnancy after delivery. Aqueous humor formation rate showed no change during pregnancy. The data indicate that the sustained elevated hormonal levels during pregnancy, either directly or indirectly, cause an increase in fluid outflow conductance from the eye without altering the rate of fluid entry.

We determined the effects of either topical or systemic calcium channel antagonists on rabbit intraocular pressure (IOP). Topical nifedipine, verapamil or diltiazem had no significant effect on IOP. Intravenous verapamil and nifedipine caused statistically significant reductions in IOP between 2 and 6 h after administration; the nifedipine response followed an increase in IOP at 30 min. Diltiazem, given 3 times daily for 3 days, caused no pressure change. In the rabbit, therefore, calcium channel antagonists have no effect when given topically, but do reduce IOP when given systemically.

The interaction between a topically administered progesterone, medrysone, and a steroid antagonist, mifepristone, on rabbit intraocular pressure (IOP) has been determined. Medrysone alone increased IOP significantly above parallel controls over the first three weeks; this increase was not sustained. When medrysone and mifepristone were given simultaneously the IOP increased initially, but then fell after two weeks to control levels. When mifepristone was added 14 days after medrysone, the IOP was again reduced to, or below, control levels by mifepristone. The use of mifepristone alone reduced IOP relative to controls and the further addition of medrysone at 14 days had no effect on IOP. It appears that mifepristone is an effective antagonist against progesterone effects on IOP.

Blood flow was measured in several tissues of the rabbit eye following intravitreal injection of a dose of endotoxin that induces an inflammatory response. In separate experiments, the vascular permeability of the inflamed eye was estimated by iris fluorescein angiography and by measuring protein influx into the aqueous humor. The effect of topical corticosteroid treatment upon blood flow and vascular permeability was also measured. Following intravitreal endotoxin injection, minor changes in blood flow occurred in retina and optic nerve head. Marked changes were observed in blood flow in iris, ciliary processes, and choroid. Steroid treatment had no effect upon the increased blood flow 24 h after the endotoxin injection, although from a clinical standpoint the steroid-treated eyes appeared less inflamed. Fluorescein angiography demonstrated a massive increase in iris vessel permeability 6 and 24 h following endotoxin injection. Topical steroid treatment reduced fluorescein entry into the anterior chamber at both time periods. On the other hand, the increase in protein influx into the aqueous humor in the endotoxin-inflamed eye was not inhibited by steroid pretreatment. It is suggested that corticosteroids have a selective effect upon the permeability of different components of the blood-aqueous barrier, namely the ciliary processes and the iris vasculature.

Studies have been made of the effects of intravitreal perfluoro-n-octane on the permeability to fluorescein of the blood-retinal barrier in rabbits. At day 1 after injection, there is increased aqueous humor fluorescence that reflects the physical disturbance to the eye following injection. From that time through 7 weeks, there is no evidence of any overt toxicity to the blood-retinal barrier. The retention in the vitreous of a small volume of perfluoro-n-octane following its intraoperative use would not be expected to induce a toxic response. Some effect on an already compromised retina cannot, however, be excluded.