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Biomedical subjects

K N Gelatt

Publications and source records attributed to K N Gelatt.

At least 19 recordsLinked to original sources
PubMed1992

Effect of hyaluronidase on aqueous outflow resistance in normotensive and glaucomatous eyes of dogs.

The anterior chambers in 16 dogs with normotensive eyes and 3 Beagles with glaucomatous eyes were treated with 0, 25, 50, or 100 IU of bovine testicular hyaluronidase. Aqueous outflow resistance was then determined by constant-pressure perfusion of 0.9% NaCl solution for 30 or 60 minutes. In normotensive eyes, 25, 50, or 100 IU of hyaluronidase significantly (P less than 0.02) increased the rate of constant-pressure perfusion compared with that of untreated eyes during 30- or 60-minute perfusions. Treatment of glaucomatous eyes with 25, 50, or 100 IU of hyaluronidase did not significantly increase the rate of constant-pressure perfusion over controls during a 30-minute perfusion. Bovine testicular hyaluronidase at all doses removed the staining of colloidal iron from the trabecular meshwork in normotensive eyes. In Beagles with glaucoma, the trabecular meshworks remained stained with colloidal iron when treated with the hyaluronidase, which suggested that some glycosaminoglycans were resistant to this enzyme's action.

Animals↗
PubMed1991

Effect of topical prostaglandin PGA2, PGA2 isopropyl ester, and PGF2 alpha isopropyl ester on intraocular pressure in normotensive and glaucomatous canine eyes.

Topical instillations of 1.0, 10, and 20 micrograms/50 microliters of prostaglandin PGA2, 0.5 and 1.0 microgram/50 microliters of PGA2 isopropyl ester, and 0.5, 1.0, 5.0 and 10.0 micrograms/50 microliters of PGF2 alpha isopropyl ester were evaluated in the normal dogs and glaucomatous beagles eyes. Each concentration of drug was evaluated for a seven day period. On Day 1 baseline values were obtained, days 2-4, the drug was instilled (once a day) and on days 5-7 post-treatment values were measured. All concentrations of PGA2 failed to lower intraocular pressure (IOP) in the normal and the glaucomatous (P greater than 0.72) dogs. PGA2 isopropyl ester decreased IOP in the normal dogs and in the glaucomatous beagles (P less than 0.01). The declines in IOP were significant at 1/2 to 1 hour and continued for up to 5 hours. No significant change in IOP occurred in the non-treated fellow eye of the normotensive dog (P less than 0.54) and the glaucomatous beagle (P less than 0.29). All concentrations of PGF2 alpha isopropyl ester significantly decreased IOP in the treated eyes of the normotensive dog (P less than 0.05) and the glaucomatous beagle (P less than 0.01). The significant change in IOP occurred within one hour after the instillation of PGF2 alpha isopropyl ester. The IOP remained lower than the baseline pressures 24 hours post-treatment for both the normotensive and glaucomatous dogs. Maximal change in IOP for normal dogs was a decrease of 9 mm Hg while the glaucomatous beagle had a decrease of 19 mm Hg. No significant change in IOP occurred in the non-treated fellow eye of the normotensive animal (P less than 0.16) and the glaucomatous beagle (P less than 0.40). The side effects of PGF2 alpha isopropyl ester were miosis and mild conjunctival irritation.

Administration, Topical↗
PubMed1991

Evaluation of a topically administered carbonic anhydrase inhibitor (MK-927) in normotensive and glaucomatous beagles.

A new topically administered anhydrase inhibitor, MK-927, was evaluated for its ocular hypotensive activity in normotensive and glaucomatous Beagles. Single- and multiple-dose studies were performed. Six concentrations of the drug were evaluated in the single-dose study and the 2% solution was used for multiple-dose evaluation. The decrease in intraocular pressure (IOP) was greater in glaucomatous Beagles at the higher concentrations of the drug. The 2 and 4% solutions of MK-927 significantly lowered IOP (mean, 5 mm of Hg; SEM +/- 1.6 and SEM +/- 1.2, respectively) in normotensive and glaucomatous Beagles. In the multiple-dose study, IOP was significantly decreased in the normotensive (mean, 4 mm of Hg; SEM +/- 0.74) and glaucomatous Beagles (mean, 9 mm of Hg; SEM +/- 1.2). The maximal effect was observed by day 4. A contralateral effect was found in glaucomatous Beagles, with the maximal effect on day 4.

Administration, Topical↗
PubMed1989

Scanning electron microscopy of corrosion casts of the optic nerve microcirculation in dogs.

Scanning electron microscopy of vascular corrosion casts of the optic nerve region in normal and glaucomatous Beagles demonstrated that the blood supply to the laminar optic nerve is derived from short posterior ciliary arteries, cilioretinal arteries, and longitudinal pial vessels. The short posterior ciliary arteries formed a ring of striated pillars around the scleral canal. The central retinal artery was not present in the dog. Differences between the casts in normal and glaucomatous dogs were not detected.

Animals↗
PubMed1989

Ultrastructural changes in laminar optic nerve capillaries of beagles with primary open-angle glaucoma.

Ultrastructural examination of optic nerve capillaries in the canine lamina cribrosa revealed many spherical, membrane-bound, electron-dense inclusions that closely resembled Weibel-Palade bodies, in pericytes and endothelial cells of preglaucomatous, early, moderately, and advanced affected Beagles with hereditary primary open-angle glaucoma. This ultrastructural difference between the laminar capillary endothelial cells of normal and glaucomatous Beagles could represent a functional vascular disorder, because Weibel-Palade bodies are associated with microcirculatory abnormalities.

Animals↗
PubMed1989

Morphologic changes in the lamina cribrosa of beagles with primary open-angle glaucoma.

Optic nerve axoplasmic flow is known to be impaired at the scleral lamina cribrosa in Beagles with hereditary primary open-angle glaucoma and is similar to the condition in human beings. Trypsin and detergent digestion to remove all neural, vascular, and glial cellular tissue revealed a well-developed scleral lamina cribrosa in the normal dog in this study. Beagles with primary open-angle glaucoma had signs of mechanical distortion of the anterior lamina cribrosa prior to the detection of ophthalmoscopic changes in the optic nerve head. This change in the supporting architecture of the optic nerve began early and increased in severity as the disease process progressed.

Animals↗
PubMed1989

Ultrastructural changes in the aqueous outflow apparatus of beagles with inherited glaucoma.

Spontaneous glaucoma in the beagle was exhibited after 6 months of age by elevated intraocular pressures and open iridocorneal angles followed by secondary changes. In order to appreciate alterations of the aqueous outflow apparatus in dogs with this autosomal recessive disorder, the eyes of beagles with inherited glaucoma at ages 1 day through 34 months were examined by light, scanning and transmission electron microscopy. Developmentally, no notable differences were observed between normal and preglaucomatous outflow channels through 7 months of age. In 12-month-old glaucomatous chamber angles clustered basement membrane-like material was found scattered throughout the outer corneoscleral trabecular meshwork. In this region elastin-like fibers appeared to be more numerous and arranged less regularly than age-matched normal eyes. Occasional trabecular cells within the corneoscleral trabecular meshwork possessed small clusters of serrated, opaque rods within their cytoplasm. In the older glaucomatous dogs these changes were more generalized and extensive throughout the entire corneoscleral trabecular meshwork. In some individual eyes the anterior chamber angles were observed to be narrow both clinically and histologically. These outflow apparatuses were additionally characterized by compressed, less organized trabeculae with a concomitant build-up of extracellular materials. No correlation was found between the shallowness of the iridocorneal angle and increase in intraocular pressure. Primary glaucoma in the beagle during its earlier phases compared more positively to open-angle glaucoma in man than any of the other spontaneous types in animals.

Animals↗
PubMed1987

Evaluation of the Krupin-Denver valve implant in normotensive and glaucomatous beagles.

The Krupin-Denver valve was implanted unilaterally in 2 normotensive and in 6 glaucomatous Beagles. The fellow eye of each dog had an external trabeculectomy. Before and after surgery, all dogs were evaluated serially by gonioscopy, biomicroscopy, tonometry, and tonography. The valve implant remained patent in 2 normotensive and in 2 glaucomatous Beagles throughout the 12 months of observation. Valve function was lost in 4 glaucomatous Beagles 4 to 6 weeks (3 dogs) and 6 months (1 dog) after implantation. Light microscopic and scanning electron microscopic evaluations of early loss of implant function revealed occlusion of the lumen and/or valve mechanism by inflammatory debris and cells. The late loss of valve function was related to chronic inflammatory response and fibrosis about the valve mechanism and tubing within the sclera.

Animals↗
PubMed1985

Quantitation of uveoscleral outflow in normotensive and glaucomatous Beagles by 3H-labeled dextran.

In uveoscleral outflow, aqueous humor leaves the anterior chamber and passes caudally through the trabecular meshwork and the sclerociliary cleft to enter the supraciliary and suprachoroidal spaces. The fluid is then absorbed by choroidal and scleral circulations. Using 3H-labeled dextran, uveoscleral outflow was quantitated in normotensive and glaucomatous Beagles under general anesthesia. The intrascleral plexus was isolated and 3H-labeled dextran was injected into the anterior chamber. Intrascleral plexus contents were sampled every 5 minutes over a 30- to 60-minute period. The eyes were enucleated, sectioned, and prepared for scintillation counting. Uveoscleral outflow accounted for 15% and 3% of the total aqueous humor outflow in the normotensive dogs and in the advanced glaucomatous dogs, respectively. In the advanced glaucomatous Beagle, conventional and uveoscleral outflow pathways were reduced and contributed to the etiopathogenesis of glaucoma.

Animals↗
PubMed1985

Morphologic studies of uveoscleral outflow in normotensive and glaucomatous beagles with fluorescein-labeled dextran.

Aqueous humor leaves the anterior chamber through 2 pathways: the trabecular meshwork of the iridocorneal angle and the unconventional uveoscleral route. In the latter route, aqueous humor leaves the anterior chamber, passes caudally through the trabecular meshwork and sclerociliary cleft to enter the supraciliary and suprachoroidal spaces. The fluid is absorbed by the choroidal and scleral circulation. Fluorescein-labeled dextran was slowly infused into the posterior chamber of healthy and glaucomatous Beagles for 30 minutes. The eyes were fixed in a mixture of 70% alcohol and formalin, placed in epoxy resin for histologic evaluation, and examined by fluorescent microscopy. Fluorescence was detected in the healthy dogs throughout the uveoscleral pathway. In the glaucomatous dogs, the uveoscleral outflow was decreased or completely absent.

Animals↗
PubMed1985

Aqueous outflow in the beagle: unconventional outflow, using different-sized microspheres.

Normal drainage of aqueous humor from the anterior chamber of the canine eye occurred through the angular aqueous plexus and uveoscleral route. In order to understand more clearly, uveoscleral outflow with regard to larger sized tracer particles and the possible influence that varying intraocular pressure (IOP) may have on them, microspheres of 3 sizes, 0.5, 1.0, and 3.0 micron, were perfused at 3 different IOP (20, 50, and 75 mm of Hg) for 3 different times (30, 60, and 90 minutes). Presence of spheres was detected by light microscopy and scanning electron microscopy, and verified by transmission electron microscopy. By 30 minutes of perfusion, all 3 sphere sizes thoroughly infiltrated the anterior uveal trabecular meshwork. At normotensive pressure (20 mm of Hg), spheres of each size penetrated the outer anterior extension of the ciliary musculature and entered the supraciliary space. Only 0.5- and 1.0-micron spheres moved posteriorly into the suprachoridal space. At hypertensive pressures, movement of the tracer particles increased markedly toward the posterior uveal trabecular meshwork. However, 3.0- and 1.0-microns spheres did not enter the supraciliary space and suprachoroidal space, respectively. Spheres also entered the iris, mostly at its root. They remained comparably sparse at different perfusion times and IOP. The present study supported evidence for uveoscleral outflow (vs uveovortex) in the dog and indicated that passage of materials through this pathway may be influenced by IOP when these substances are within a critical size range.

Animals↗
PubMed1979

Cataracts in Chesapeake Bay Retrievers.

Cataracts developed in 13 of 27 related Chesapeake Bay Retrievers. The posterior pole, "Y" sutures, and equatorial cortices of the lens were predominantly affected. In one affected dog, the cataracts had progressed to hypermaturity, permitting restoration of vision. The trait was believed to be dominant, with incomplete penetrance.

Age Factors↗
PubMed1979

Ocular hypotensive effects of carbonic anhydrase inhibitors in normotensive and glaucomatous Beagles.

Four carbonic anhydrase inhibitors (acetazolamide, dichlorphenamide, ethoxzolamide, and methazolamide) cause ocular hypotony in normotensive and glaucomatous Beagles. Four dosages of acetazolamide and methazolamide and three dosages of dichlorphenamide and ethoxzolamide were evaluated. The extent of ocular hypotony after these carbonic anhydrase inhibitors was usually greater in glaucomatous Beagles than it was in normotensive Beagles.

Acetazolamide↗
PubMed1979

Evaluation of a soluble sustained-release ophthalmic delivery unit in the dog.

A 5-mg hydroxypropyl cellulose soluble ocular insert was evaluated by placement in the upper and the lower conjunctival and bulbar nictitating membrane fornices in normal dogs. The insert was easily placed in the conjunctival fornices, but was difficult to place in the bulbar nictitating membrane fornix. The conjunctival inserts did not produce irritation of the cornea and the conjunctiva. Placement of the inserts beneath the nictitating membrane produced local irritation and chemosis. The sites of highest to lowest retention for the insert were upper conjunctival fornix, bulbar nictitating membrane fornix, and lastly, lower conjunctival fornix. Dissolution was nearly complete in 8 hours.

Animals↗
PubMed1979

Uveoscleral flow of aqueous humor in the normal dog.

Fluorescein-labeled dextran and sodium fluorescein perfused in the posterior chamber of the normal dog eye egressed through the trabecular meshwork and intrascleral plexus, as well as posteriorly through the ciliary body into the suprachoroidal space and the sclera. Intraocular pressures of 20, 25, 30, and 60 mm of Hg did not produce detectable changes in the fluorescein-labeled dextran movement. Topical 1% atropine and 10% phenylephrine did not affect posterior passage of sodium fluorescein; 2% pilocarpine impeded posterior passage, causing an accumulation of sodium fluorescein and associated fluorescence in the anterior ciliary body.

Animals↗