Effect of intraocular pressure on uveoscleral outflow following cyclodialysis in the monkey eye

Cyclodialysis was performed in both eyes of five cynomolgus monkeys. Two days later the intraocular pressure (IOP) had fallen from 17.7 +/- 0.8 to 7.1 +/- 1.4 mm Hg (P less than 0.001). At that time, both eyes were perfused for 30 min with fluorescein-isothiocyanate (FITC) dextran (MW 70,000), one at 35 mm Hg and the other at 4 mm Hg. Four pairs of control eyes (without cyclodialysis) were perfused in the same manner. At 4 mm Hg, uveoscleral outflow was 0.02 +/- 0.02 microliter/min in control eyes and 0.05 +/- 0.04 microliter/min in eyes following cyclodialysis. However, at 35 mm Hg, uveoscleral outflow in eyes with cyclodialysis increased to 2.13 +/- 0.47 microliters/min compared to 0.32 +/- 0.10 microliter/min in control eyes. Thus the "facility" of uveoscleral outflow in control eyes is 0.01 microliter/min/mm Hg and in eyes following cyclodialysis is 0.07 microliter/min/mm Hg. It is concluded that cyclodialysis results in a pressure-dependent increase in uveoscleral outflow.     

Different Effects of Topical Prazosin and Pilocarpine on Uveoscleral Outflow in Rabbit Eyes

Purpose:To investigate the effects of topical prazosin and pilocarpine on uveoscleral outflow(Fu) in rabbits.Methods:Sixteen rabbits were randomly divided into the control group (5 rabbits, only topical application of normal saline in the fight eye of each rabbit), Prazosin (PZ) treated group (6 rabbits, only 0.1％ Prazosin eyedrop 0.1％ in the right eye of each one) and Pilocarpine (PC) treated group (5 rabbits, 1％ Pilocarpine eye drop in each fight eye). Intraocular pressure (IOP) of bilateral eyes of each rabbit was measured before and 1h after topical application of the eye drop. And the bilateral eyes were perfused with Fluorescein-isothiocyanate bovine serum albumin (FITC-BSA) as the tracer into the anterior chamber of each rabbit for 30 min at 90 min after topical treatment. Then the rabbits were killed for Fu measurement.Results:IOP of PZ-treated eyes decreased [(0.71±0.07)kPa] in 1 hour after PZ application. IOP of PC-treated eyes decreased [(0.70±0.08)kPa] in 1 hour after PC application. Th     

Outflow of aqueous humor following cyclodialysis or ciliochoroidal detachment in rabbit

Cyclodialysis and ciliochoroidal detachment were performed in three eyes of three rabbits and in three eyes of another three rabbits, respectively. After aspiration of the aqueous humor, 0.1 ml of 10% sodium fluorescein was injected intracamerally, and the eyeball was enucleated between 30 minutes and one hour after injection and prepared for fluorescence microscopy. Sodium fluorescein concentrations in the supraciliary space were much greater in the group with cyclodialysis or ciliochoroidal detachment than in the normal control group. These results suggest that (1) in the eye with cyclodialysis, the aqueous humor may freely gain access to the supraciliary space through the cleft between the anterior chamber and the supraciliary space and then be removed rapidly and (2) in the eye with ciliochoroidal detachment, the aqueous humor may pass through the uveoscleral outflow pathway.     

Aqueous humor dynamics in experimental iridocyclitis

Ocular inflammation was induced by intravitreal bovine serum albumin (BSA) injection in one eye of each of six cynomolgus monkeys. The fellow eyes were injected with sterile saline alone. The intraocular pressure decreased by 12.2 +/- 1.3 mmHg (mean +/- SE) 2 days after BSA injection and 4.0 +/- 1.1 mmHg after saline injection. Aqueous flow and uveoscleral outflow were determined with fluorescein isothiocyanate (FITC) dextran 70. Aqueous flow in inflamed eyes averaged 0.32 +/- 0.04 ul/min, less than half the rate of control eyes (0.77 +/- 0.08 ul/min, P = 0.01). The facility of uveoscleral outflow in inflamed eyes was four times that of control eyes (0.2 +/- 0.03 vs 0.05 +/- 0.01 ul/min/mmHg, respectively, P = 0.009). Fluorescence microscopic examination revealed intense fluorescence of the edematous ciliary body muscle and of the suprachoroidal space extending to the posterior pole. These findings indicate that BSA-induced ocular inflammation causes a simultaneous reduction in aqueous humor flow and an increase in uveoscleral outflow, resulting in ocular hypotony.     

Uveoscleral outflow using different-sized fluorescent tracers in normal and inflamed eyes

Sodium fluorescein and fluorescinated dextrans (FD) of selected molecular weights were combined and perfused into the anterior chamber of normal and inflamed eyes of cynomolgus monkeys. The eyes were dissected into iris, anterior and posterior uvea, anterior and posterior sclera, retina and intraocular fluids (excluding aqueous). Each tissue was homogenized and centrifuged and the supernatant was run through a gel-filtration column to separate the fluorescent tracers. Each of the resultant peaks was quantitated and facility of uveoscleral outflow was determined. In control eyes the calculated facility of uveoscleral outflow was very similar with all tracers (from 0.047-to 0.052 microliter min-1 mmHg-1) and each tracer was found in highest concentration in the anterior sclera and anterior uvea. In inflamed eyes the calculated facility of uveoscleral outflow increased two- to five-fold with each tracer (0.12-; 0.17-; 0.29-; and 0.24 microliter min-1 mmHg-1 with fluorescein, and the fluorescinated dextrans of MWs 4000, 40,000 and 150,000, respectively). Each tracer was found in the anterior sclera and uvea in inflamed eyes whereas the posterior sclera and uvea contained predominantly the higher molecular-weight tracers (MWs 40,000 and 150,000). It is concluded that iridocyclitis causes an increase in uveoscleral outflow by increasing the permeability of the anterior uvea to all tracers and fluid. Small tracers may then diffuse into uveal blood vessels or across the sclera, yielding lower values for uveoscleral outflow. Of the four tracers studied, the optimal tracer size for studying uveoscleral outflow in either normal or inflamed eyes is MW 40,000.     

A method for near-continuous determination of aqueous humor flow; effects of anaesthetics, temperature and indomethacin

A method is described for near-continuous determination of aqueous humor flow. The anterior chamber is perfused with push-pull coupled syringes at a low rate with a fluid containing labelled albumin. An external circuit is used to determine continuously the anterior chamber concentration of the labelled protein. The dilution data are analysed on-line by a minicomputer which permits rapid calculation of the anterior chamber volume and the rate of flow of aqueous humor. The technique and some experiments of technical interest are reported. Experiments in monkeys with different anaesthetics resulted in flow values of 0.99 +/- 0.02, 1.47 +/- 0.09 and 0.99 +/- 0.04 microliter min-1 for pentobarbital, urethane and ketamine anaesthesia, respectively. By using 125I-labelled albumin in one eye and 131I-labelled albumin in the other, it was possible to determine flow in both eyes. Highly significant correlation coefficients between the two sides were found for the rate of aqueous flow, intraocular pressure and anterior chamber volume. Rapid changes in inflow into the anterior chamber from the posterior chamber were produced by elevating and then lowering the intraocular pressure; the delay inherent in the method was about 6 min. Indomethacin, 3 mg kg-1 body wt., had no effect on aqueous humor flow in eyes cannulated with a minimum of trauma. In eyes with problematic cannulation indomethacin at this dose tended to delay an irritation response. Changes in temperature of the fluid perfused through the anterior chamber had no clear effect on the rate of aqueous flow. Warming the animals about 3-4 degrees C above the normal temperature tended to increase the rate of aqueous flow. Cooling by 3-4 degrees C had no clear effect. Cooling after an initial warming also had no clear effect. The rate of flow of aqueous humor from the anterior chamber to the general circulation was calculated from data for the accumulation of labelled albumin in the general circulation. The difference between the rate of aqueous flow determined from the dilution data and the flow into blood was assumed to represent uveoscleral flow. In 14 animals with an aqueous flow of 1.19 +/- 0.08 microliters min-1 the flow to the general circulation was 0.57 +/- 0.055 and uveoscleral flow 0.61 +/- 0.09 microliters min-1. The procedure and mathematical treatment will be applicable to flow determinations with other large molecules and in other systems.     

Uveoscleral outflow: diffusion or flow?

Shallow peripheral ciliochoroidal detachments with 10(-4) M fluorescein isothiocyanate dextran 70 were created in cynomolgus monkey eyes. Anterior chamber fluorophotometric readings were taken for 6 hr. From the anterior chamber fluorescence values, the rate of tracer movement from the supraciliary space into the anterior chamber was calculated. The rate of movement was 0.003 microliter/min, expressed in equivalent volumes of tracer solution. This value is more than 200 times lower than the rate of tracer movement from the anterior chamber to the supraciliary space. It is concluded that tracer movement from the anterior chamber to the supraciliary space (uveoscleral route) results from fluid flow rather than diffusion.     

Effect of topical pergolide on aqueous dynamics in normal and glaucomatous monkeys

The effects of pergolide mesylate, an ergoline derivative, were studied on intraocular pressure (IOP), outflow facility, aqueous humor flow, and pupil size in monkeys. Unilateral topical administration of two 20-microliters drops of 0.1% pergolide significantly lowered IOP in the treated- and contralateral eye in both normal- and glaucomatous monkeys. In 12 normal monkeys, the baseline IOP of 18.3 +/- 0.4 mmHg [mean +/- S.E.(M.)] was maximally reduced to 14.4 +/- 0.7 mmHg in the treated eye (P less than 0.001) and 14.6 +/- 0.6 mmHg in the contralateral eye (P less than 0.001) at 2 hr after drug administration. In 10 monkeys made bilaterally glaucomatous by argon laser treatment of the trabecular meshwork, the baseline IOP of 33.9 +/- 3.0 mmHg [mean +/- S.E.(M.)] in the treated eyes and 31.7 +/- 3.3 mmHg in the untreated eyes maximally decreased to 23.9 +/- 2.2 mmHg (P less than 0.05) and 26.2 +/- 3.3 mmHg (P less than 0.005), respectively, at 5 hr. No significant change (P greater than 0.7) in outflow facility occurred in either eye of 11 normal monkeys 2 hr after unilateral 0.1% pergolide treatment. In six normal monkeys, the baseline aqueous humor flow of 1.58 +/- 0.20 microliter min-1 in treated eyes and 1.44 +/- 0.18 microliter min-1 in untreated eyes was reduced to 0.92 +/- 0.08 microliter min-1 (P less than 0.02) and 1.09 +/- 0.11 microliter min-1 (P greater than 0.10), respectively, from 0.5- to 3.5 hr after drug administration. A mydriatic response was observed in both eyes after unilateral treatment from 1- to 2 hr in eight normal monkeys. By the third day of treatment, bilateral twice a day 0.1% pergolide drops in eight glaucomatous monkey eyes no longer significantly (P greater than 0.05) decreased IOP.     

Perfusate effects upon resistance to aqueous humor outflow in the rhesus monkey eye. A comparison of glutathione-bicarbonate Ringer's solution to pooled aqueous humor as perfusate.

In vivo perfusion of the anterior chamber of normal rhesus monkeys with pooled rhesus aqueous humor gives an initial total facility of 0.48 +/- 0.08 (+/-S.E.) microliter/min/mm Hg. With continued intermittent perfusion for 2 hr this value increased only slightly to 0.57 +/- 0.10 microliter/min/mm Hg. Perfusion of the paired eyes of the same monkeys with glutathionebicarbonate Ringer's solution gives an initial total facility of 0.55 +/- 0.08 microliter/min/mm Hg. This value increased to 1.21 +/- 0.15 microliter/min/mm Hg with continued intermittent perfusion. Thus aqueous is a satisfactory perfusate for experiments requiring prolonged stability of the eye, but glutathione-bicarbonate Ringer's solution is not a satisfactory substitute perfusate. Neither addition of physiologic amounts of ascorbic acid to the buffered salt solution nor careful modification of the pH of the solution to the physiologic level prevented the increase of total facility it produces when used as a perfusate. A reversible, fast-phased small-magnitude increase in total facility was noted in eyes perfused with either perfusate. It is speculated this is caused by neural mechanisms for intraocular pressure control.     

Effects of brinzolamide on aqueous humor dynamics in monkeys and rabbits.

This study examines the mechanisms by which brinzolamide reduces intraocular pressure (IOP) in healthy rabbits and in monkeys with unilateral ocular hypertension. Intraocular pressures were measured by pneumatonometry and aqueous flow was determined by fluorophotometry before and after three twice-daily drops of 1% brinzolamide to both eyes per monkey and after similar treatment to one eye per rabbit. In monkeys, outflow facility was determined by fluorophotometry and uveoscleral outflow was calculated. In rabbits, outflow facility was determined by two-level constant pressure infusion and uveoscleral outflow was measured by an intracameral tracer technique. Compared with contralateral vehicle-treated rabbit eyes, IOP was reduced in brinzolamide-treated eyes by 2.5 +/- 1.9 mmHg (mean +/- standard deviation; p =.006) at four hours after the second dose. Aqueous flow was reduced by 0.50 +/- 0.65 microl/min (p =.02). This effect was found in rabbits previously treated with brinzolamide but not in naive rabbits. Treated hypertensive eyes of monkeys had a reduction in IOP of 7.3 +/- 8.8 mmHg (p = 0.01) and aqueous flow of 0.69 +/- 1.10 microL/min (p = 0.05) when compared with baseline. Brinzolamide did not affect outflow facility or uveoscleral outflow in either rabbits or monkeys. It is concluded that, in normotensive eyes of rabbits and hypertensive eyes of monkeys, brinzolamide reduces IOP by reducing aqueous flow and not by affecting aqueous humor drainage.     

Prostaglandin F2 alpha increases uveoscleral outflow in the cynomolgus monkey

Cynomolgus monkeys were treated topically in one eye twice daily with prostaglandin F2 alpha-l-isopropylester (PGF2 alpha-IE) for nine doses. On treatment day 4, 3 hr after the seventh dose, intraocular pressure (IOP) in the treated eye was reduced by 65% compared to the controls, to less than 5 mmHg. On treatment day 5, 3 hr after the ninth dose, total outflow facility was determined by two-level constant pressure perfusion of the anterior chamber. Immediately thereafter, uveoscleral outflow was determined by intracamerally infusing [125I]- or [131I]-albumin and fluoresceinated dextran, and calculating the volume of anterior chamber fluid required to have deposited the quantity of tracer recovered from the various ocular and periocular tissues. Simultaneously, trabecular outflow was determined by calculating the volume of anterior chamber fluid required to have deposited the quantity of tracer recovered from the general circulation. Total facility was approximately 50% higher in treated than in control eyes, but the effect was variable, of marginal statistical significance, and perhaps due to increased pseudofacility or uveoscleral facility. Uveoscleral outflow was approximately two to three-and-a-half times higher in treated than in control eyes, the magnitude of the effect being dependent upon the timing and pressure at which the perfusion was conducted. Trabecular outflow was reduced by approximately 75% in the treated eyes relative to control so that the proportion of total outflow comprised by trabecular outflow in the treated eyes was only one third that in the controls. Total aqueous flow was slightly (approximately 20%) but not significantly reduced in the treated eyes. The IOP lowering effect of PGF2 alpha in the cynomolgus monkey is due largely if not exclusively to an increase in uveoscleral outflow of aqueous humor, with aqueous outflow being redirected from the trabecular to the uveoscleral route.     

眼调节对葡萄膜巩膜房水外流途径影响的形态学观察

目的　通过形态学观察探讨眼调节对葡萄膜巩膜房水外流途径的影响。方法　14只健康日本大耳白兔,10只（20眼）用于荧光显微镜观察,4只（8眼）用于光镜观察,按用药方法不同各分为调节状态组和非调节状态组。所有白兔双眼分别采用5 g·L^-1硝酸毛果芸香碱滴眼液和10 g·L^-1盐酸环喷托酯滴眼液模拟眼调节态和非调节态,测量滴眼前及末次滴眼后30 min的眼压,于滴眼后30 min将5 μL异硫氰酸荧光素标记牛血清白蛋白（FITC-BSA）注入前房,于前房注射后0.5 h、1.5 h、2.5 h、3.5 h、4.5 h各处死2只白兔,摘取双眼作冰冻切片,于荧光显微镜下观察调节态和非调节态葡萄膜巩膜途径的房水荧光强度及其分布形态;于滴眼后30 min处死4只白兔,摘取双眼通过HE染色和抗平滑肌抗体染色在普通光镜下观察兔眼睫状肌形态、肌间隙。结果　调节状态组基线眼压（19.13±1.75）mmHg（1 kPa=7.5 mmHg),毛果芸香碱模拟眼调节后眼压下降,滴眼后眼压为（16.56±1.67）mmHg,差异有统计学意义（t=9.37,P=0.00)。调节状态组睫状体、脉络膜上腔和前巩膜荧光强度较非调节状态组均显著减弱（均为P<0.05）,而两组间后巩膜、脉络膜差异均无统计学意义（均为P＞0.05）。光镜观察见非调节状态组放射肌区域有明显肌间隙,而在调节状态组未发现此间隙。结论　眼调节可通过收缩睫状肌从而减少房水从葡萄膜巩膜房水外流道排出。     

Effects of a prostaglandin DP receptor agonist, AL-6598, on aqueous humor dynamics in a nonhuman primate model of glaucoma.

This study examines, in 11 cynomolgus monkeys with unilateral laser-induced glaucoma, the ocular hypotensive mechanism of action of AL-6598, partial agonist at the DP and EP prostanoid receptors. In a crossover fashion, both eyes of each monkey were dosed twice daily with 25 microL of either AL-6598 0.01% or vehicle for 2 days and on the morning of the 3rd day. Measurements were made on day 3 of each treatment. Alternative treatments were separated by at least 2 weeks. Intraocular pressures (IOPs) were measured by pneumatonometry and aqueous flow and outflow facility by fluorophotometry. Uveoscleral outflow was calculated mathematically. In the normotensive eyes, compared to vehicle treatment, AL-6598 decreased IOP from 22.5 +/- 0.7 to 18.7 +/- 0.9 mmHg (P = 0.006), increased uveoscleral outflow from 0.47 +/- 0.17 to 1.22 +/- 0.17 microL/min (P = 0.03), and increased aqueous flow from 1.49 +/- 0.10 to 1.93 +/- 0.13 microL/min (P = 0.01). No measurement in AL-6598-treated hypertensive eyes was significantly different from vehicle treatment. It is concluded that AL-6598 reduces IOP by increasing uveoscleral outflow in normotensive eyes of ketamine-sedated monkeys, despite an increase in aqueous flow. This effect is different from that of PGD(2), which decreases aqueous flow, and of the selective DP receptor agonist, BW245C, which increases both outflow facility and uveoscleral outflow in addition to decreasing aqueous flow.     

New Management of Angle—closure Glaucoma by Phacoemulsification with Foldable Posterior Chamber Intraocular Lens Implantation

Objective: To investigate the management oi angle-closure glaucoma byphacoemulsification with foldable posterior chamber intraocular lens (PC-IOL)implantation.Design: Retrospective, noncontrolled interventional case series.Participants: In 36 eyes with angle-closure glaucoma (ACG) , there were 18 eyes withprimary acute angle-closure glaucoma (PACG) , 14 eyes with primary chronicangle-closure glaucoma (PCCG) , 3 eyes with secondary acute angle-closure glaucoma(SACG) and 1 eye with secondary chronic angle-closure glaucoma (SCCG).Intervention: Phacoemulsification with posterior chamber intraocular lens implantation.Main Outcome Measures: Postoperative visual acuity, IOP, axial anterior chamberdepth.Results: After a mean postoperative follow-up time of 8. 81±7. 45 months, intraocularpressure was reduced from a preoperative mean of 23. 81 ±17. 84 mmHg to apostoperative mean of 12. 54 4. 73 mmHg ( P =0. 001). Mean anterior chamber depthwas 1. 75 ± 0. 48 mm preoperatively and 2. 29 ?0. 38 mm postoperatively     

A simple photogrammetric method of measuring anterior chamber volume.

We devised a convenient method of measuring anterior chamber volume in man. Photographs of the anterior chamber were taken with a Zeiss photographic slit lamp with a Polaroid attachment, and measured with a specially constructed transparent scale. Using this method, the standard deviation of individual measurements of volume on different occasions in a given eye was 8 microliter. The standard deviation of the differences between right and left eyes of normal subjects was 10 microliter. The volume of the anterior chamber measured in 78 eyes of 39 normal subjects (mean age, 28 years; range, 19 to 56 years) was found to be 209 +/- 37 microliter (mean +/- SD). We observed a small negative correlation between the age of the subject and the volume of the anterior chamber.     

A comparison of the intraocular pressure-lowering effect and safety of viscocanalostomy and trabeculectomy with mitomycin C in bilateral open-angle glaucoma

PURPOSE: To compare the intraocular pressure-lowering effect and safety of viscocanalostomy and trabeculectomy with mitomycin C. METHODS: Twenty-five patients with bilateral primary open-angle glaucoma were enrolled in a prospective clinical study. The eyes of each patient were randomly assigned to receive viscocanalostomy in one eye and trabeculectomy with mitomycin C in the other eye. The patients were followed up for 12 months. At each visit, best-corrected visual acuity, intraocular pressure, and the appearance of the surgical wound, anterior chamber, and indirect ophthalmoscopy were recorded. RESULTS: The mean baseline intraocular pressure was 25.0+/-2.2 mmHg in viscocanalostomy-treated eyes and 24.8+/-2.6 mmHg in trabeculectomy-treated eyes. The mean postoperative intraocular pressure was 15.3+/-1.7 mmHg, 17.1+/-1.5 mmHg, and 17.1+/-1.5 mmHg in viscocanalostomy-treated eyes and 11.7+/-4.4 mmHg, 11.8+/-4.6 mmHg, and 12.6+/-4.3 mmHg in trabeculectomy-treated eyes at 3-, 6- and 12-month intervals, respectively. The mean intraocular pressure in viscocanalostomy-treated eyes was significantly higher than that in trabeculectomy-treated eyes at every visit (P<0.0001). At 12 months, 16 viscocanalostomy-treated eyes (64%) and 22 trabeculectomy-treated eyes (88%) achieved an intraocular pressure of less than or equal to 20 mmHg without medication; there was a significant difference between the two groups (P=0.0240). There were fewer complications in viscocanalostomy-treated eyes. Complications included four cases of shallow anterior chamber (16%) and five of hypotony (20%) in trabeculectomy-treated eyes, against intraoperative microperforation of Descemet's membrane in one of viscocanalostomy-treated eye (4%). CONCLUSION: Trabeculectomy with mitomycin C may be more effective than viscocanalostomy in lowering intraocular pressure in patients with primary open-angle glaucoma, while eyes undergoing viscocanalostomy experience a lower incidence of complications. Further investigation of more cases is needed.     

Effects of multiple dosing of epinephrine on aqueous humor dynamics in human eyes.

Numerous studies have provided conflicting evidence to explain the ocular hypotensive mechanism of action of epinephrine. Although epinephrine has been shown consistently to increase outflow facility, its effects on aqueous flow and uveoscleral outflow are not as clear. The purpose of this study was to clarify the effects of multiple doses of topical epinephrine on aqueous humor dynamics in human eyes. This was done by evaluating the four main parameters that determine steady state intraocular pressure. These parameters were assessed at baseline and after a week of twice-daily treatment of epinephrine hydrochloride 2% to one eye. Twenty-six human volunteers were enrolled in the study. Intraocular pressure was measured by pneumatonometry, aqueous flow and trabecular outflow facility by fluorophotometry, episcleral venous pressure by venomanometry and uveoscleral outflow by mathematical calculation. In epinephrine-treated eyes compared to baseline, intraocular pressure and aqueous flow were reduced from 21.2 +/- 0.3 to 17.1 +/- 0.2 mmHg (19%, p = .01) and 3.3 +/- 0.2 to 2.9 +/- 0.2 microl/min (12%, p = .03), respectively. Trabecular outflow facility obtained by fluorophotometry was increased from 0.18 +/- 0.02 to 0.26 +/- 0.03 microl/min/mmHg (44%, p = .02). Topical epinephrine did not significantly affect uveoscleral outflow or episcleral venous pressure. In conclusion, multiple topical doses of epinephrine lowered intraocular pressure in human volunteers by reducing aqueous humor formation and increasing trabecular outflow facility. The increase in uveoscleral outflow suggested by other studies was not observed.     

Effect of apraclonidine in long-term timolol users.

A double-blind, randomized study was undertaken to determine if the alpha-agonist apraclonidine has an additive effect in eyes treated with long-term timolol. Seventeen patients (15 with primary open-angle glaucoma, 1 with pigmentary glaucoma, and 1 glaucoma suspect) on long-term timolol treatment in both eyes received a single dose of apraclonidine in one eye and a placebo in the other. Aqueous flow and intraocular pressure were compared in the treated and untreated eyes. There was no statistically significant difference in pretreatment aqueous flow between the two eyes. When flow in the apraclonidine-treated eyes (1.39 +/- 0.41 microliter/min, mean +/- standard deviation) was compared with that of the untreated eyes (1.66 +/- 0.38 microliter/min), a statistically significant difference was found (P less than 0.01). Apraclonidine reduced intraocular pressure by 1.3 mmHg (P = 0.05). The implications of these findings on the understanding of the mechanism of action of adrenergic drugs in the human eye is discussed.     

Aqueous dynamics in exfoliation syndrome.

Eighteen untreated patients with unilateral exfoliation syndrome without glaucoma were studied with regard to differences in aqueous dynamics between the affected and unaffected fellow eyes. Additionally, both eyes of the patients with exfoliation were compared to the eyes of 18 age-matched and gender-matched control subjects. Intraocular pressure was significantly higher (13.9 +/- 3.0 mm Hg [mean +/- standard deviation]) in the affected compared with the unaffected eyes (12.2 +/- 2.5 mm Hg), but no difference in aqueous humor flow was detected when eyes in the three groups were compared (affected eyes, 2.40 +/- 0.60 microliter/min; unaffected eyes, 2.40 +/- 0.65 microliter/min; control eyes, 2.61 +/- 0.60 microliter/min). Anterior chamber volumes were significantly smaller in affected (122 +/- 37 microliters) and unaffected eyes (121 +/- 37 microliters) of the patients with exfoliation compared with the eyes of the control subjects (145 +/- 30 microliters). Apparent resistance was higher in the eyes with exfoliation (6.5 +/- 1.9 min mm Hg/microliters) compared with both unaffected (5.4 +/- 1.2 min mm Hg/microliters) and control groups (5.2 +/- 1.8 min mm Hg/microliters), although these differences were not statistically significant.     

Ocular rigidity evaluation after photorefractive keratectomy: an experimental study

PURPOSE: To evaluate possible changes of the ocular rigidity coefficient in vivo after photorefractive keratectomy (PRK) in a series of rabbit eyes, using an invasive ocular rigidity measurement device. METHODS: Sixteen eyes of 8 rabbits were used in this study. One eye from each rabbit underwent PRK for -10.00 diopters (D) in a 5-mm optical zone (92 microm) while the fellow eye served as the control. Five weeks later, the rabbits were examined under general anesthesia. The pressure-volume relationship and the ocular rigidity coefficient were determined in all 16 eyes, by injecting 200 microL of saline solution (in increments of 4.5 microL) through the limbus into the anterior chamber, while the intraocular pressure (IOP) was continually monitored with a transducer, up to a maximum limit of 40 mmHg. Data within an IOP range of 10 to 40 mmHg were used to calculate the ocular rigidity coefficient. RESULTS: The preoperative central corneal thickness was comparable (P = .73, paired t test) in the pre-PRK eyes (mean: 347.5 +/- 17.11 microm) and control eyes (mean: 349.1 +/- 17.46 microm). No statistically significant difference was noted in measured ocular rigidity coefficient between eyes treated with PRK and control eyes (mean rigidity coefficient: 0.42 +/- 0.12 mmHg/microL [range: 0.23 to 0.56] and 0.47 +/- 0.12 mmHg/microL [range: 0.28 to 0.62], respectively, with 95% confidence interval of the difference, lower: -0.10 to upper: 0.015, P = .121). CONCLUSIONS: Photorefractive keratectomy did not significantly alter ocular rigidity measurements in this experimental model.