Literature DB >> 1463422

Juxtacanalicular tissue in pigmentary and primary open angle glaucoma. The hydrodynamic role of pigment and other constituents.

C G Murphy1, M Johnson, J A Alvarado.   

Abstract

We tested the hypothesis that obstruction of the juxtacanalicular tissues, by melanin granules in pigmentary glaucoma and by other impermeable material in primary open angle glaucoma, leads to the development of a chronic glaucomatous condition. The distribution and concentration of melanin and other impermeable materials in the juxtacanalicular tissues and elsewhere in the trabecular meshwork was determined in 13 specimens. Six specimens were from patients with pigmentary glaucoma, two from patients with pigment dispersion syndrome, and three from patients with primary open angle glaucoma, as well as two from normal subjects. The effect of these materials on flow resistance was estimated using two hydrodynamic models. In model A, the electron-lucent spaces of the juxtacanalicular tissue were assumed to be open spaces, while in model B, these spaces and spaces filled with ground substance were assumed to be gel filled. In pigmentary glaucoma, 3.5% of the pigment was found in the juxtacanalicular tissue, while 96.5% was found in the corneoscleral and uveoscleral tissues. Permeabilities calculated according to model A were much higher than those expected from estimates of outflow facility in all groups, in agreement with the previous report of Ethier et al. The gel-filled spaces available for fluid flow, as determined by model B, showed no statistically demonstrable differences (pigmentary glaucoma, 32.9%; primary open angle glaucoma, 36.6%; pigment dispersion syndrome, 43.4%; normal, 44.1%). Furthermore, the amount of pigment present in the juxtacanalicular tissue was determined to have a negligible influence on permeability. Thus, the development of the chronic glaucomatous condition cannot be directly attributed to pigment accumulation in the juxtacanalicular tissue in pigmentary glaucoma.

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Year:  1992        PMID: 1463422     DOI: 10.1001/archopht.1992.01080240119043

Source DB:  PubMed          Journal:  Arch Ophthalmol        ISSN: 0003-9950


  17 in total

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3.  Interactions between endothelia of the trabecular meshwork and of Schlemm's canal: a new insight into the regulation of aqueous outflow in the eye.

Authors:  Jorge A Alvarado; Ru-Fang Yeh; Linda Franse-Carman; George Marcellino; Michael J Brownstein
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4.  Ultrastructural changes associated with dexamethasone-induced ocular hypertension in mice.

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5.  Dexamethasone inhibition of trabecular meshwork cell phagocytosis and its modulation by glucocorticoid receptor beta.

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Review 6.  The changing paradigm of outflow resistance generation: towards synergistic models of the JCT and inner wall endothelium.

Authors:  Darryl R Overby; W Daniel Stamer; Mark Johnson
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7.  ETIOLOGY OF IOP ELEVATION IN PRIMARY OPEN ANGLE GLAUCOMA.

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8.  Mitochondrial damage in the trabecular meshwork occurs only in primary open-angle glaucoma and in pseudoexfoliative glaucoma.

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9.  An imaged-based inverse finite element method to determine in-vivo mechanical properties of the human trabecular meshwork.

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Journal:  J Model Ophthalmol       Date:  2017

10.  Marfan syndrome caused by a novel FBN1 mutation with associated pigmentary glaucoma.

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