The effects of topical pilocarpine on the morphology of the outflow apparatus of the baboon (Papio cynocephalus).
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The morphology of the outflow system of the baboon (Papio cynocephalus) was studied by light microscopy and transmission electron microscopy in tissue from eyes treated with topical pilocarpine. In one group of five animals the intraocular pressure (IOP) was maintained at 18 mm /g in both the experimental and the control eye of each baboon for the duration of the experiment. The endothelial meshwork was more distended, and there was a significantly greater number of giant vacuoles in the lining endothelium of Schlemm's canal in the pilocarpine-treated eyes than in the corresponding controls. However, in another series of animals, IOP was not maintained, and the differences between the treated and untreated eyes was much less striking. There appeared to be little evidence that the increase in vacuolation was produced by the direct action of pilocarpine on the endothelium of Schlemm's canal; more likely, it was a consequence of an increased passage of fluid through the drainage system. In addition, we have been able to show that (1) the mode of primary fixation can produce partial reversal of the pilocarpine effect and (2) the mechanical manipulation which is required to determine outflow facility has a deleterious effect on the morphology of the outflow tissues. (+info)
A light microscopic study of the effects of testicular hyaluronidase on the outflow system of a baboon (Papio cynocephalus).
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An attempt was made to investigate the effects of hyaluronidase on the morphology of the baboon outflow system. The eyes of six adult baboons provided the material for this histological study. For each animal the IOP in both eyes was maintained at 18 mm Hg, and 150 IU of testicular hyaluronidase were introduced into one eye and a control solution into the other. It was observed by light microscopy that the outer meshwork was more distended in the hyaluronidase-treated outflow system than in the corresponding controls. Further, it was found from a quantitative analysis that the incidence of giant vacuoles in the endothelium of Schlemm's canal was greater in the experimental than the control eye of each animal. The difference between the vacuole counts in the experimental and control eyes was significant in five of the six animals. These preliminary findings provide morphological evidence which indicates that there is a hyaluronidase-sensitive barrier to aqueous outflow in the baboon drainage system. (+info)
Multivariate approach for quantification of morphologic and functional damage in glaucoma.
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PURPOSE: To determine the usefulness of confirmatory factor analysis in examination of morphometric, electrophysiological, and psychophysical quantitative methods that measure the extent of global glaucomatous damage without referring to a preselected gold standard. METHODS: In a cross-sectional clinical study, 406 eyes of 203 glaucoma patients and 200 eyes of 100 normal control subjects 18 to 70 years old underwent optic disc morphometry, automated perimetry, measurement of temporal contrast sensitivity by a full-field flicker test, blue-on-yellow visually evoked potential (VEP), and black-and-white pattern-reversal electroretinogram (ERG). Diagnosis of glaucoma was based on a qualitative classification of the optic nerve head and retinal nerve fiber layer independent of intraocular pressure and visual field. Confirmatory factor analysis was performed in the patient group as a whole and in a subgroup showing moderate to advanced glaucomatous optic nerve head damage. RESULTS: The confirmatory factor analysis models explained the data satisfactorily (P > 0.18, all patients; P > 0.34, subgroup). Global glaucomatous damage was quantified best by the mean defect of automated perimetry (r = 0.81; r = 0.87), followed by the area of the neuroretinal rim (r = 0.64; r = 0.73), the full-field flicker test (r = 0.59; r = 0.65), the pattern-reversal ERG amplitude (r = 0.54; r = 0.55), and the VEP peak time (r = 0.55; r = 0.54). CONCLUSIONS: Confirmatory factor analysis allows quantification of the validity of established and new procedures that measure global glaucomatous damage using cross-sectional data. The results are not dependent on the preselection of a specific gold standard. Psychophysical testing and morphometry quantified glaucomatous damage best, compared with electrophysiological procedures. (+info)
Effect of nitric oxide synthase inhibitor on optic nerve head circulation in conscious rabbits.
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PURPOSE: To study the effect of a nitric oxide synthase inhibitor on tissue circulation in the optic nerve head (ONH) of conscious rabbits. METHODS: N(G)-nitro-L-arginine methyl ester (L-NAME) (1, 10, or 100 mg/kg), D-NAME (10 mg/kg), or physiological saline was administered intravenously to albino rabbits. A quantitative index of blood velocity, the normalized blur (NB), was measured in the ONH by laser speckle tissue circulation analyzer. The intraocular pressure (IOP) and blood pressure (BP) were also measured. L-arginine (10 mg/kg) was intravenously administered 20 minutes after L-NAME (10 mg/kg) injection. Acetylcholine (ACh; 10 microg/kg per minute) was infused for 15 minutes, with or without pretreatment of L-NAME (1 mg/kg). RESULTS: L-NAME induced a continuous decrease of the NB in a dose-dependent manner, but D-NAME caused no significant change. At 100 mg/kg, L-NAME significantly increased the IOP, mean BP, and ocular perfusion pressure, but the other doses caused no significant changes. When L-arginine was administered after L-NAME injection, the NB returned to its initial level and remained there. Pretreatment with L-NAME inhibited the increase of NB induced by ACh. CONCLUSIONS: These results indicate that nitric oxide regulates basal tissue circulation in the ONH of conscious rabbits and suggest that ACh increases the circulation by promoting nitric oxide synthesis. (+info)
The efficacy of 0.2% brimonidine for preventing intraocular pressure rise following argon laser trabeculoplasty.
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Brimonidine tartrate of 0.5% was identified as the most effective and safe dose for acute intraocular pressure (IOP) lowering. The efficacy of brimonidine tartrate 0.2% in preventing IOP elevation after an argon laser trabeculoplasty (ALT) was evaluated. Eighty patients were selected for a randomized, prospective study. Each patient was assigned to one of four treatment regimens: (1) brimonidine before and after ALT(B/B), (2) brimonidine before and placebo after ALT(B/P), (3) placebo before and brimonidine after ALT(P/B), (4) placebo before and after ALT(P/P). IOP elevation of 5 mmHg or greater occurred in 3.3% (2/60) of brimonidine-treated patients and in 30% (6/20) of placebo-treated patients. There was a mean decrease of IOP from baseline during the first 3 hours after ALT in all brimonidine-treated groups (7.1 +/- 3.4, 6.2 +/- 4.4, 3.5 +/- 2.9 mmHg for the B/B, B/P, P/B groups), but no change of mean IOP in the Placebo-treated group. Only one drop of brimonidine tartrate of 0.2% installed either before or after ALT was sufficient to prevent post-ALT IOP spike and minimize the undesired systemic adverse effects that two drop installation can produce. (+info)
Haploinsufficiency of the transcription factors FOXC1 and FOXC2 results in aberrant ocular development.
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Anterior segment developmental disorders, including Axenfeld-Rieger anomaly (ARA), variably associate with harmfully elevated intraocular pressure (IOP), which causes glaucoma. Clinically observed dysgenesis does not correlate with IOP, however, and the etiology of glaucoma development is not understood. The forkhead transcription factor genes Foxc1 (formerly Mf1 ) and Foxc2 (formerly Mfh1 ) are expressed in the mesenchyme from which the ocular drainage structures derive. Mutations in the human homolog of Foxc1, FKHL7, cause dominant anterior segment defects and glaucoma in various families. We show that Foxc1 (+/-)mice have anterior segment abnormalities similar to those reported in human patients. These abnormalities include small or absent Schlemm's canal, aberrantly developed trabecular meshwork, iris hypoplasia, severely eccentric pupils and displaced Schwalbe's line. The penetrance of clinically obvious abnormalities varies with genetic background. In some affected eyes, collagen bundles were half normal diameter, or collagen and elastic tissue were very sparse. Thus, abnormalities in extracellular matrix synthesis or organization may contribute to development of the ocular phenotypes. Despite the abnormalities in ocular drainage structures in Foxc1 (+/-)mice, IOP was normal in almost all mice analyzed, on all genetic backgrounds and at all ages. Similar abnormalities were found in Foxc2 (+/-)mice, but no disease-associated mutations were identified in the human homolog FKHL14 in 32 ARA patients. Foxc1 (+/-)and Foxc2 (+/-)mice are useful models for studying anterior segment development and its anomalies, and may allow identification of genes that interact with Foxc1 and Foxc2 (or FKHL7 and FKHL14 ) to produce a phenotype with elevated IOP and glaucoma. (+info)
Secondary anterior crocodile shagreen of Vogt.
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The clincopathological features and pathogenesis of secondary mosaic degeneration of the cornea (anterior crocodile shagreen of Vogt) are described. The structural basis for the normal anterior corneal mosaic pattern seems to lie in the particular arrangement of many prominent collagen lamellae of the anterior stroma that thake an oblique course to gain insertion into Bowman's layer. Since, at normal intraocular pressure, Bowman's layer is under tension, when viewed from the anterior surface the cornea appears smooth. By releasing the tension, however, a reproducible polygonal ridge pattern becomes manifest. It is suggested that a prolonged phthisical state of the eye is one condition wherein the mosaic pattern may become permanent and that, as a secondary event, this is followed by irregular calcification of Bowman's layer which particularly involves the ridges projecting into the epithelium. Biomicroscopically these ridges corresponded to the branching reticular arrangement of the mosaic opacities. (+info)
Experimental glaucoma and cell size, density, and number in the primate lateral geniculate nucleus.
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PURPOSE: To examine the effects that elevated intraocular pressure (IOP), a glaucoma risk factor, has on the size, density, and number of neurons in the primate lateral geniculate nucleus (LGN). METHODS: The monkey model of experimental glaucoma was combined with standard histologic staining and analysis techniques. Fourteen animals were examined. RESULTS: Mean IOPs higher than 40 mm Hg for 2.5, 4, 8, and 24 weeks resulted in reductions of 10% to 58% in the cross-sectional areas of LGN neurons receiving input from the glaucomatous eye. Reductions for animals with lower mean IOPs (37 and 28 mm Hg) for 16 and 27 weeks were 16% and 30%, respectively. Neurons receiving input from the normal eye also were reduced in size (4 -26%). No differential effect in cell size was seen for magnocellular versus parvocellular neurons. Elevation of IOP resulted in an increase in cell density in all layers of the LGN. The increase was approximately two times greater in parvocellular (59%) than magnocellular (31%) layers. When corrected for volumetric shrinkage of the LGN, the estimated loss of neurons was approximately four times greater in the magnocellular than parvocellular layers (38% versus 10%). CONCLUSIONS: Elevation of IOP affects the size, density, and number of neurons in the LGN, and the volume of the nucleus itself. Although higher mean pressures (more than 40 mm Hg) reduce the period during which these changes occur, comparable damage can be achieved by even moderate (28 -37 mm Hg) levels of elevated IOP. On the basis of cell loss, elevation of IOP appears to have a more profound degenerative effect on the magnocellular than on the parvocellular regions of the LGN. (+info)