Effect of body position on intraocular pressure and aqueous flow.

The relationship between intraocular pressure and the rate of aqueous humor formation was studied in human subjects. Intraocular pressure was altered by changing the subject's gravity-dependent body position. Aqueous humor flow was measured fluorophotometrically. An average change of intraocular pressure of 2.4 +/- 1.2 mmHg and 11.2 +/- 2.7 mmHg was recorded in subjects whose body position was alternated +/- 15 degrees from horizontal and +/- 50 degrees from horizontal. No change of the rate of fluorescein clearance was observed for the milder change of position. A small change of fluorescein clearance was noted in response to the steeper change of position. Changing intraocular pressure seems not to induce compensatory changes in aqueous flow. Therefore we conclude that aqueous formation is relatively pressure-insensitive, a conclusion one would draw from clinical instances of angle-closure glaucoma or as in other systems of secretion, such as the toad bladder or the cerebrospinal fluid, where alterations in pressure do not necessarily influence flow. If there is a regulator of aqueous flow it is not responsive to the changes in intraocular pressure brought about in this study. If aqueous flow regulates intraocular pressure or compensates for changes in intraocular pressure, the signal is not small changes in pressure.

Effects of timolol, epinephrine, and acetazolamide on aqueous flow during sleep.

The effects of timolol, epinephrine, and acetazolamide on the rate of flow of aqueous humor through the anterior chamber of awake and sleeping human subjects was studied. Timolol reduced the rate in awake subjects but not sleeping subjects. Epinephrine increased the rate in sleeping subjects to a greater extent than in awake subjects. Acetazolamide reduced the rate of flow in awake subjects or epinephrine-stimulated subjects. Acetazolamide reduced the rate of flow slightly below the basal rate observed during sleep, but the reduction was small and not statistically significant. The authors propose that the diurnal fluctuation of the rate of aqueous humor flow in humans is driven by changes in the concentration of endogenous epinephrine available to the ciliary epithelia.

Measurement of aqueous humor flow with scanning ocular fluorophotometers.

A one-dimensional scanning fluorophotometer (Fluorotron Master) and a two-dimensional scanning fluorophotometer (McLaren and Brubaker) were used to measure rate of aqueous humor flow in normal volunteers. The precision of three protocols of dye application and flow determination was investigated. In all three protocols rate of flow was determined by observing the rate of disappearance of topically-applied fluorescein during an 8-hour period. The three protocols studied were: 1) Two drops of 10% fluorescein washed away five minutes later immediately before beginning measurements of fluorescence. 2) Application of 0.25% fluorescein every 5 minutes for 30 minutes, 6 hours before beginning measurements. 3) Iontophoresis for 7 seconds and irrigation of eye immediately before beginning measurements. Rate of flow was calculated by the methods of Jones and Maurice. The results were compared to measurements made with a slit-lamp fluorophotometer using the technique described by Coakes and Brubaker. The most satisfactory method of measuring flow when either scanning fluorophotometer was employed was to instill fluorescein many hours before measurements begin (protocol 2).

Aqueous humor flow during sleep.

The rate of aqueous humor flow of 19 normal subjects was measured by a fluorescein clearance technique during the day, during sleep (at night) and during sleep deprivation (at night). Subjects engaged in routine activities during the daytime measurements and slept in comfortable quarters during the nighttime measurement. They remained awake and active during the sleep deprivation study. The nomographic method of Coakes and Brubaker , a method in which the subject is not disturbed at all during the critical 5-hr period, was used to calculate flow. Flow was lower during sleep in all but one subject. The range of nighttime flow suppression was 8% to 68% in all of the other subjects with a mean suppression of 45% +/- 20%. Aqueous flow was lower at night even when the subjects were awake but was lowest during sleep at night. The reduction of aqueous flow during sleep is comparable with the suppression that can be achieved with carbonic anhydrase inhibitors or beta adrenergic blockers.

Effect of clonidine on aqueous humor flow in normal human eyes.

A randomized, double-blind, placebo-controlled study of the effect of topical 0.125% clonidine, a relatively specific alpha 2-adrenergic agonist, on the rate of aqueous humor flow in the eyes of 24 normal human subjects was performed with fluorophotometry. The effect of clonidine on intraocular pressure, anterior chamber volume, pupil size, pulse, and blood pressure was also studied. Clonidine-treated eyes had a 2 mmHg decrease in intraocular pressure which was statistically significant. Fellow placebo-treated eyes had a smaller but significant decrease in pressure. However, between clonidine and fellow placebo-treated eyes, no significant difference was found in intraocular pressure. Aqueous humor flow was 21% lower in clonidine-treated eyes as compared to fellow placebo-treated eyes, 1.9 microliter min-1 as compared to 2.4 microliters min-1. No significant difference was found in anterior chamber volume, blood-aqueous barrier diffusion constant, and apparent resistance between clonidine and fellow placebo-treated eyes. Clonidine produced a significant miosis of 0.4 mm in treated eyes and miosis of 0.2 mm in fellow eyes. Topical 0.125% clonidine significantly decreased systolic blood pressure by 3 mmHg, but did not affect diastolic blood pressure or pulse.