Search PubMed⌕ Search

Biomedical subjects

J E Pederson

Publications and source records attributed to J E Pederson.

At least 19 recordsLinked to original sources
PubMed1991

Glaucoma. A primer for primary care physicians.

Glaucoma is best detected by examination of the optic disk, since intraocular pressure is not always elevated in patients with the condition. A large, vertically oval cup within the optic disk is strong evidence for glaucoma. Open-angle glaucoma, the most common form of the disorder, often is not detected until the disease is advanced. It can usually be treated successfully with topical medications, but systemic absorption of these can result in serious side effects. If medical treatment fails, laser therapy or filtering surgery may be helpful. Acute angle-closure glaucoma has a sudden onset marked by alarming elevations in intraocular pressure. It is treated immediately with topical pilocarpine and systemic osmotic agents, and an iridectomy should be performed as soon as possible. Congenital glaucoma can be cured with goniotomy.

Family Practice↗
PubMed1990

Extravascular albumin concentration of the uvea.

The hypothesis that uveal vessels absorb fluid was tested by measuring the albumin in extravascular uveal tissues and in plasma. From these results the effective albumin concentration was calculated in both rabbits and monkeys. Three separate methods were used to measure uveal albumin, and the results of these were compared. In method 1, the intravenous fluorescein isothiocyanate (FITC)-albumin concentration found in the uvea 5 min after injection (intravascular tracer) was subtracted from that found 2 hr after injection (intravascular plus extravascular tracer) to determine the extravascular albumin concentration. In method 2, intravenous FITC-albumin was followed by vascular washout after a 2-hr equilibration period to determine extravascular uveal albumin. In method 3, the endogenous extravascular albumin concentration of uveal tissues was measured with an enzyme-linked immunosorbent assay (ELISA) after vascular washout. The effective albumin concentration was determined by dividing the data in methods 1, 2, and 3 by the extravascular albumin space volume. The effective albumin concentration in monkey (as percentage of plasma) was, for methods 1, 2, and 3: iris 2, 3, and 4%; pars plicata 14, 12, and 7%; pars plana 2, 10, and 12%; and choroid 2, 12, and 10%, respectively. In rabbit, the extravascular albumin concentrations were: iris 10, 21, and 7%; pars plicata 69, 26, and 39%; pars plana 41, 46, and 10%; and choroid 88, 30, and 26%, respectively. These findings are lower than previously reported in rabbits, yet are consistent with previous estimates in monkeys. These results support the hypothesis that uveal vessels are capable of fluid absorption, since a large colloid osmotic gradient exists across the vessel wall.

Albumins↗
PubMed1989

Hydrostatic pressure of the suprachoroidal space.

The hydrostatic pressure of the suprachoroidal space was measured in 18 cynomolgus monkey eyes by one of two methods: (1) direct cannulation, or (2) silicone sponge implantation. The intraocular pressure (IOP) and suprachoroidal pressure were monitored simultaneously with the IOP being held at various levels between 5 and 60 mm Hg. In eyes with direct cannulation, at an IOP of 15 mm Hg, the pressure in the anterior suprachoroidal (supraciliary) space was 0.8 +/- 0.2 mm Hg (n = 6, mean +/- SE) below the IOP, but the posterior suprachoroidal pressure was 3.7 +/- 0.4 mm Hg (n = 8) below the IOP. The suprachoroidal pressure in eyes with silicone sponge implant was 4.7 +/- 0.6 (n = 7) mm Hg below the IOP. A change in IOP produced a corresponding change in the supraciliary space pressure. However, the pressure difference between the anterior chamber and the posterior suprachoroidal space increased at higher IOP. This pressure differential is the driving force for uveoscleral outflow.

Animals↗
PubMed1988

Volume flow across the isolated retinal pigment epithelium of cynomolgus monkey eyes.

The retinal pigment epithelium (RPE)-choroid was isolated from cynomolgus monkey eyes with experimental retinal detachments and the volume flow was determined in vitro using Ussing-type chambers. With zero pressure difference across the membrane, retina-to-choroid volume flow was 5.0 microliter/hr/cm2 in eyes with subacute retinal detachments (1-2 weeks). In eyes with chronic retinal detachment (8-20 months), the flow was 7.3 microliter/hr/cm2. Volume flow was not affected by the elimination of ambient bicarbonate. Transepithelial potential difference and resistance were 8.9 mV, retinal side positive, and 339 ohm-cm2, respectively, in chronic retinal detachments. It is concluded that there is a posteriorly directed flow of fluid across the RPE in cynomolgus monkey eyes with chronic retinal detachments.

Animals↗
PubMed1988

Effect of plasma osmolality and intraocular pressure on fluid movement across the blood-retinal barrier.

The inward permeability of the blood-retinal barrier to carboxyfluorescein was determined in monkey eyes with and without rhegmatogenous retinal detachment (RD). In the absence of changes in the diffusional permeability of the retinal pigment epithelium (RPE), inward permeability changes reflect changes in fluid flow across the RPE. Intravenous injection of mannitol resulted in a 15 mosmol/kg increase in plasma osmolality which decreased inward permeability 37% in eyes with RD and 21% in eyes with vitrectomy alone. When the intraocular pressure was raised 20 mm Hg above normal, inward permeability decreased 29% in eyes with RD and 32% in normal eyes. It is concluded that fluid flow across the blood-retinal barrier is influenced by both plasma osmolality and intraocular pressure.

Animals↗
PubMed1987

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.

Animals↗
PubMed1987

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.

Animals↗
PubMed1987

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.

Animals↗
PubMed1987

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.

Animals↗
PubMed1987

Acetazolamide effect on the inward permeability of the blood-retinal barrier to carboxyfluorescein.

The inward permeability of the blood-retinal barrier to carboxyfluorescein was determined in 12 cynomolgus monkeys. Probenecid (175 mg/kg), an inhibitor of active outward transport of carboxyfluorescein, did not affect the inward permeability, indicating that the inward permeability is independent of the active outward transport system. However, acetazolamide (20 mg/kg), which causes increased outward fluid movement across the retinal pigment epithelium (RPE), significantly reduced the inward permeability. Thus, inward diffusion of carboxyfluorescein interacts with outward fluid flow across the RPE. Since carboxyfluorescein has low lipid solubility and remains extracellular, it is concluded that the pathway of fluid movement and carboxyfluorescein diffusion across the RPE is paracellular.

Acetazolamide↗
PubMed1987

Permeability of the blood-retinal barrier to carboxyfluorescein in eyes with rhegmatogenous retinal detachment.

Outward and inward permeability of carboxyfluorescein across the blood-retinal barrier were measured fluorophotometrically in seven cynomolgus monkey eyes with experimental rhegmatogenous retinal detachment. Probenecid was used to inhibit outward transport of carboxyfluorescein. The outward permeability was 1.98 +/- 0.31 microliter/min in eyes with retinal detachment and 0.84 +/- 0.15 microliter/min in control eyes with vitrectomy alone (P less than 0.01). The inward permeability, determined separately following intravenous injection, was significantly lower than the outward permeability: 0.14 +/- 0.02 microliter/min for eyes with retinal detachment and 0.04 +/- 0.01 microliter/min for control eyes. Since the outward permeability minus the inward permeability in the presence of probenecid represents that fraction of tracer moving due to fluid flow, it may be concluded that outward flow of fluid across the blood-retinal barrier is a substantial contributor to carboxyfluorescein loss from the vitreous cavity following intravitreal injection.

Animals↗
PubMed1986

Experimental retinal detachment. XI. Furosemide-inhibitable fluid absorption across retinal pigment epithelium in vivo.

Rhegmatogenous retinal detachments were created in one eye of each of six cynomolgus monkeys. Total vitrectomy alone was performed in the fellow eyes. The rate of disappearance of fluorescein sodium injected into the vitreous cavity was measured with kinetic vitreous fluorophotometry. Intravitreal 10(-4)M probenecid was used to inhibit active outward transport of fluorescein. In eyes with retinal detachment, the rate of fluorescein loss from the vitreous cavity was decreased 44% and 22% following intravitreal injection of 10(-4) and 10(-5)M furosemide (Lasix), respectively. Intravitreal 10(-4)M furosemide decreased the rate of fluorescein loss in fellow eyes by 35%. The rate of fluorescein loss via the anterior chamber accounted for only 1% to 8% of the total rate of vitreous fluorescein loss. Thus, it is concluded that intravitreal absorption across the retinal pigment epithelium.

Absorption↗
PubMed1986

Ocular hypotony.

In hypotony, where the intraocular pressure is lower than the episcleral venous pressure, aqueous humour outflow must be via unconventional channels, such as uveoscleral outflow pathways. The level of intraocular pressure will be determined by the rate of aqueous humour production and the facility of unconventional outflow. The facility of unconventional outflow has been shown to be increased in eyes with experimentally-induced hypotony from cyclodialysis, ciliochoroidal detachment, iridocyclitis, or retinal detachment. Aqueous humour production is reduced in eyes with hypotony during the acute phase following cyclodialysis, and in eyes with iridocyclitis or rhegmatogenous retinal detachment. Chronic cyclodialysis or ciliochoroidal detachment does not lead to reduced aqueous humour production, if unassociated with iridocyclitis. Detachment of the ciliary body in hypotony is often associated with, but does not appear to cause, reduced aqueous humour formation. Apart from treatment of the specific cause of hypotony, reduction of the accompanying inflammatory response is essential for normalisation of aqueous dynamics and intraocular pressure.

Animals↗
PubMed1986

Permeability of the isolated dog retinal pigment epithelium to carboxyfluorescein.

Outward (retina to choroid) and inward (choroid to retina) permeabilities of carboxyfluorescein and fluorescein in the isolated dog retinal pigment epithelium (RPE)-choroid were determined. Outward permeability was 9 and 47 times larger than inward permeability for carboxyfluorescein and fluorescein, respectively. The outward permeability of carboxyfluorescein was seven times lower than that of fluorescein, whereas there was no statistical difference between the inward permeabilities. Carboxyfluorescein is thus distinguished from fluorescein by its low affinity to the outwardly directed organic anion transport system. 10(-4) M probenecid caused greater than 98% inhibition of the outward transport of 6 X 10(-5) M carboxyfluorescein and 6 X 10(-6) M fluorescein.

Animals↗
PubMed1985

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.

Animals↗
PubMed1985

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.

Animals↗
PubMed1985

Experimental retinal detachment. X. Effect of acetazolamide on vitreous fluorescein disappearance.

Retinal detachments were created in one eye of each of eight cynomolgus monkeys. Total vitrectomy was performed in the fellow eyes. Fluorophotometry was used to study the rate of disappearance of fluorescein injected into the vitreous cavity. The rate of fluorescein loss via the anterior chamber accounted for only 1% to 3% of the total rate of vitreous fluorescein loss in eyes with retinal detachment or in fellow eyes. Posterior loss of fluorescein (presumably across the retinal pigment epithelium) increased by 25% following intravenous acetazolamide in eyes with retinal detachment and 22% in fellow eyes. It is concluded that acetazolamide increases the rate of fluid absorption across the retinal pigment epithelium.

Acetazolamide↗