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Cheryl R Hann

Publications and source records attributed to Cheryl R Hann.

3 recordsLinked to original sources

Cationic ferritin and segmental flow through the trabecular meshwork.

PURPOSE: To determine whether segmental labeling by the tracer molecule cationic ferritin (CF) is indicative of preferential patterns of fluid flow in the trabecular meshwork or of differences in cell and extracellular matrix properties. Nonlabeled regions could indicate no fluid entering that area, insufficient perfusion time, or that the cells and extracellular matrix differ in that region and cannot bind CF. METHODS: Six whole eyes (three normal and three with pseudoexfoliation [PEX]) syndrome were perfused with CF for 30 minutes to 4 hours. Wedges of trabecular meshwork were dissected and some wedges immediately fixed. Adjacent wedges were placed in a CF bath before fixation. Transmission electron microscopy was used to analyze CF labeling. RESULTS: CF increased in the trabecular meshwork with increasing perfusion time. At 30 minutes, CF labeled mainly the uveal and corneoscleral regions. By 4 hours, CF was found diffusely through the meshwork, although a few isolated nonlabeled areas were still present. Wedges immersed in the CF bath showed fewer nonlabeled regions at all time points. Clumps of PEX material labeled more heavily in the periphery than the center, suggesting the clumps were less permeable than surrounding regions. PEX eyes otherwise had similar labeling patterns. CONCLUSIONS: Segmental labeling with CF implies regions of preferential flow exist in the meshwork. With increasing perfusion time, there were fewer nonlabeled regions. CF labeling of most regions of bath-immersed tissue suggests that nonlabeled regions do not differ in the characteristics of the cells, but rather that CF does not reach these regions.

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Pharmacologic disruption of Schlemm's canal cells and outflow facility in anterior segments of human eyes.

PURPOSE: To determine the effect of disruption of Schlemm's canal cells on outflow facility. Pharmacologic agents that weaken the cytoskeleton or interfere with integrin binding may allow targeted disruption of the cells lining Schlemm's canal because of the transmural pressure gradient the cells face as aqueous passes into the canal. METHODS: Anterior segments of human eyes were placed in perfusion organ culture, and either single or sequential doses of H-7 or RGD peptide were added. Fellow eyes received vehicle or RGE peptide. Eyes were fixed and examined by light and electron microscopy. RESULTS: Both agents caused a partial loss of the endothelial lining of Schlemm's canal cells without disruption of trabecular cells in other regions. H-7 significantly increased outflow facility after single or sequential doses, with moderate cell loss of both the inner and outer wall canal cells: 20.0% +/- 10.5% of the width of the canal versus 5.2% +/- 3.7% in control meshworks (P = 0.05). No significant correlation between the amount of canal cell loss and outflow facility was found. RGD was associated with a variable loss of canal cells but did not change outflow facility. CONCLUSIONS: Pharmacologic disruption of Schlemm's canal cells appears possible. H-7 increased outflow facility, causing a partial loss of the endothelial lining of Schlemm's canal. A simple relationship between canal cells and outflow facility was not found; canal cells probably interact with the extracellular matrix in influencing outflow facility.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

Factors influencing intraocular pressure in cultured human anterior segments.

PURPOSE: To determine why variations in intraocular pressure (IOP) occur in cultured human anterior segments despite a constant rate of infusion of culture medium. Two types of variations occur: an initial elevation of IOP and small changes in baseline IOP. METHODS: Anterior segments from human eyes were placed in perfusion organ culture. In cultures with initially high IOP, eyes were fixed at the high IOP level and histologic examination performed. In other cultures with high initial IOP, effluent medium was collected and subsequently reinfused after IOP had decreased to baseline. In cultures with stable baseline IOP, cell fragments from monolayer-cultured cells, or human genomic DNA, were infused at concentrations equivalent to 30,000 to 300,000 cells. RESULTS: Electron microscopy of initially high-pressure cultures revealed scattered cell debris throughout the meshwork in greater amounts than found in eyes without initially high IOP. Reinfusion of effluent media from cultures with high initial pressures caused elevation of IOP. Centrifugation of effluent media lessened this elevation of IOP. In cultures with stable baseline IOP, infusion of cell fragments or genomic DNA raised IOP in a dose-dependent manner, with elevation of IOP for a minimum of 24 hours. CONCLUSIONS: Cell debris can elevate IOP during the initial culture period, and after baseline pressures are established. Cell fragments and DNA increase IOP in a dose-dependent manner. The variations in baseline IOP seen during culture are probably caused by cell fragments and debris from dying cells in the meshwork, ciliary body, and other anterior segment tissues.

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