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C B Toris

Publications and source records attributed to C B Toris.

26 records · Page 2Linked to original sources

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.

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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.

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Functional recovery of retinal pigment epithelial damage in experimental retinal detachment.

The integrity of the RPE barrier function in retinal detachment was studied in vitro. The retinal pigment epithelium (RPE)-choroid tissue was isolated from cynomolgus monkey eyes with acute (less than 1 hr), subacute (1-2 weeks), and chronic (8-20 months) retinal detachments, and clamped between Ussing-type chambers. Electrical characteristics and choroid-to-retina permeability to carboxyfluorescein were determined. In the HEPES-buffered bathing solution, transepithelial potential difference and resistance in eyes with acute retinal detachments (0.2 mV and 134 ohm-cm2, respectively) were significantly lower than subacute (7.9 and 350) and chronic (10.4 and 348) retinal detachments. Furthermore, the permeability was increased five-fold in acute retinal detachments with respect to subacute and chronic retinal detachments, indicating a breakdown of the RPE barrier in acute retinal detachment. No statistical difference was found between subacute and chronic retinal detachments. In this animal model, RPE barrier function is destroyed at the onset of retinal detachment, but recovers in a week or two, and is maintained in the chronic stage. Histological examination revealed that RPE recovery was accomplished by RPE proliferation and hyperplasia.

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Experimental retinal detachment. VIII. Retinochoroidal horseradish peroxidase diffusion across the blood-retinal barrier.

Unilateral rhegmatogenous retinal detachments in 13 cynomolgus monkeys were studied with horseradish peroxidase (HRP). When injected subretinally in six eyes, HRP did not diffuse anteriorly into the sensory retina and penetrated posteriorly through the zonulae occludentes of the retinal pigment epithelium (RPE) in only two eyes. In seven eyes, tracer was detected after intravitreal HRP injection throughout the sensory retina, the basal lamina of retinal blood vessels, and the subretinal space, but did not penetrate through the RPE. In 13 control eyes (with vitrectomy), intravitreal HRP penetrated the sensory retina and the basal lamina surrounding inner retinal blood vessels. These results confirm that the zonulae occludentes of the RPE and retinal blood vessels remain intact in most eyes after rhegmatogenous retinal detachment. Furthermore, the HRP staining patterns suggest a posteriorly directed movement of fluid across the RPE and possible fluid absorption by retinal blood vessels.

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Experimental retinal detachment. IX. Aqueous, vitreous, and subretinal protein concentrations.

Unilateral rhegmatogenous retinal detachments were created in seven cynomolgus monkeys. Six months later, aqueous, vitreous, and subretinal fluid protein concentrations were measured. In fellow eyes with vitrectomy alone, mean aqueous and vitreous protein concentrations were 0.28 and 0.23 mg/mL, respectively. In eyes with retinal detachments, mean aqueous, vitreous, and subretinal protein levels were 1.46, 2.66, and 4.74 mg/mL, respectively. Eyes with a large retinal hole (greater than or equal to 1 disc diameter) had a subretinal fluid-vitreous protein concentration ratio of 1.1, indicating free diffusional exchange between the vitreous and subretinal space. In eyes with a small retinal hole (less than or equal to 1/4 disc diameter), the corresponding ratio was 4.0. These findings are consistent with the hypothesis that fluid moves from the vitreous cavity through the retinal hole into the subretinal space, preventing back diffusion of protein from the subretinal space into the vitreous, and allowing accumulation of protein in the subretinal space.

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Uveoscleral outflow following cyclodialysis in the monkey eye using a fluorescent tracer.

Cyclodialysis was performed in one eye of each of eight cynomolgus monkeys. Two days later, the intraocular pressure was 1.6 +/- 0.7 mmHg in eyes with cyclodialysis and 12.0 +/- 0.7 mmHg in fellow control eyes. 10(-4) M fluorescein-isothiocyanate dextran (70,000 molecular weight) was perfused into the anterior chamber of each eye for 30 min. The eyes were enucleated and dissected into sclera, choroid, retina, iris, and ocular fluid. Samples were homogenized and centrifuged, and the fluorescence of the supernatant was measured. Expressed as equivalent volumes of aqueous, the rate of anterior chamber movement of tracer via uveoscleral pathways was 1.40 +/- 0.17 microliter/min in cyclodialysis eyes and 0.34 +/- 0.10 microliter/min in control eyes. Cyclodialysis results in a fourfold increase in uveoscleral outflow, contributing to the observed hypotony.

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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.

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Experimental retinal detachment. VII. Intravenous horseradish peroxidase diffusion across the blood-retinal barrier.

Intravenous horseradish peroxidase (HRP) was administered to cynomolgus monkeys to study chorioretinal diffusion in eyes with retinal detachment. In control eyes, HRP was contained within the choriocapillaris and did not penetrate beyond Bruch's membrane. In addition, HRP was confined within blood vessels of the sensory retina. In detached eyes, HRP diffused out of the choriocapillaris and through the intercellular spaces of the retinal pigment epithelium (RPE), where it was blocked by zonulae occludentes. Occasionally HRP was found within pinocytotic vesicles of the RPE. It was also confined within retinal blood vessels by their endothelial cells. It is concluded that the blood-retinal barrier remains intact to HRP following long-term rhegmatogenous retinal detachment. However, a slight alteration exists at the choriocapillaris in detached eyes.

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