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Biomedical subjects

T M Richardson

Publications and source records attributed to T M Richardson.

23 records · Page 2Linked to original sources

Distribution of glycosaminoglycans in the aqueous outflow system of the cat.

Although glycosaminoglycans (GAGs) have been postulated to play a role in the regulation of intraocular pressure, structural localization of specific varieties of GAGs in the outflow system is necessary before their precise role can be determined. In this study, the outflow system of the cat was stained with ruthenium red to identify GAGs with the electron microscope. The composition of the ruthenium red-stainable material was determined by predigestion of tissues with testicular hyaluronidase, neuraminidase, or papain. Testicular hyaluronidase-sensitive GAGs were located on the surfaces of the endothelial cells in the trabecular meshwork and aqueous plexus, within their basal laminae, and in the amorphous tissue of the trabecular beams and tissue adjacent to the aqueous plexus. Collagen and elastic fibers throughout the outflow system were also associated with ruthenium red-stainable material that was resistant to testicular hyaluronidase. Connective tissue GAGs, but not endothelial cell-associated GAGs, were demonstrated to be complexed to protein, since they were disrupted by papain treatment. Neuraminidase-sensitive material (sialoglycoprotein) was identified only on the lumenal surface of the endothelial cells of the aqueous plexus. The complex distribution of GAGs and order polyanions in the outflow system of the cat suggests that the these macromolecules may serve more than one function.

Animals↗

Exfoliation glaucoma: a quantitative perfusion and ultrastructural study.

The aqueous outflow systems of both eyes from a patient with well documented exfoliation syndrome were studied postmortem by quantitative perfusion and scanning and transmission electron microscopy. This provided a rare opportunity to correlate clinical and postmortem findings. the right eye was phakic with early glaucoma. The left eye was aphakic with moderately severe glaucoma prior to the cataract surgery. The eyes were fixed at a perfusion pressure of 25 mm Hg. In both eyes the spaces of the corneoscleral trabecular meshwork were open and mostly free of exfoliation material. The trabecular cells appeared normal and contained no exfoliation material. Failure to take up exfoliation material contrasts with the known tendency of these cells to take up pigment and other particles. The main pathology involved destruction of Schlemm's canal and accumulation of exfoliation material in the juxtacanalicular region of both eyes. The changes in Schlemm's canal and the juxtacanalicular region appeared sufficient to account for increase in resistance to aqueous outflow.

Aged↗

Corneal decompensation in Chandler's syndrome. A scanning and transmission electron microscopic study.

A corneal button obtained from a 58-year-old woman with Chandler's syndrome was studied by light and electron microscopy. Clinically, the patient had mild unilateral glaucoma, slight changes in the iris, endothelial dystrophy, and corneal edema that was increasingly sensitive to intraocular pressure. Corneal pathology included loss of large numbers of endothelial cells with consequent exposure of Descemet's membrane. Endothelial cells demonstrated irregular shape, partial loss of tight junctions, and increased numbers of cytoplasmic filaments. Some endothelial cells appeared metaplastic or perhaps were replaced by cells from some source other than the cornea. Proliferation of cells was not apparent. A thin layer of acellular tissue, containing long-spacing collagen and 15-nm-wide fibrils, was interposed between normal Descemet's membrane and the endothelium. These observations suggest a basis for the corneal edema that distinguishes Chandler's syndrome from other forms of essential iris atrophy.

Cornea↗

The outflow tract in pigmentary glaucoma: a light and electron microscopic study.

Buttons obtained by trephination from both eyes of a 44-year-old myopic man with pigmentary glaucoma were studied by light and electron microscopy. Although clinically both eyes exhibited heavy pigmentation of the trabecular meshwork in the whole circumference, microscopically the trabecular meshwork of the left eye contained more pigment granules than that of the right eye, which appeared relatively acellular with collapse of the trabecular sheets. In both eyes endothelial cells covering the trabecular sheets were filled with pigment and showed various stages of degeneration. The intertrabecular spaces contained free pigment granules as well as cell debris. These observations suggest that plugging of the trabecular spaces by pigment and cell debris together with fragmentation and collapse of trabecular sheets contribute to the decrease in the facility of outflow that occurs in pigmentary glaucoma.

Endothelium↗