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Biomedical subjects

T Tokura

Publications and source records attributed to T Tokura.

26 records · Page 2Linked to original sources

[Morphological study of experimental corneal neovascularization after anterior uveal ischemia].

We morphologically investigated what kinds of inflammatory cells infiltrate the corneoscleral limbus by light and electron microscopy and what manner of keratocytes and vascular endothelial cells appear at the corneal limbus, when the corneal edema was aggravated severely and clinical corneal new vessels were found initially, i.e. until three days after anterior segmental ischemia in rabbit eyes. The majority of infiltrating inflammatory cells were polymorphonuclear leukocytes and the others were lymphocytes and histiocytes etc. Peripheral keratocytes around limbal vessels were stimulated and transformed to fibroblastic cells as a result of anterior segment ischemia. Proliferating endothelial cells of comparatively minor limbal vessels invaded between corneal lamellar layers toward the corneal center. Polymorphonuclear leukocytes were often found near activated keratocytes proliferating vascular endothelial cells, hear and there. Consequently, it is considered that the stimulated polymorphonuclear leukocytes play an important role when corneal neovascularization occurs after anterior segmental ischemia.

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[Morphological study of corneal edema after anterior segment ischemia].

This experiment was performed to investigate the correlation between morphological changes of the corneal endothelium and clinical corneal edematous opacities after a procedure causing obstruction of bilateral long posterior ciliary arteries of the albino-rabbits. Shortly after the procedure, corneal endothelium became irregular on the anterior-chamber side and there were numerous lysosomal granules in the cytoplasm of corneal endothelial cells. On the third day, endothelial cells became necrotic and collapsed and a part of the cells peeled into the anterior chamber. Fibroblast-like cells and inflammatory cells were piled up in severely damaged areas of the endothelium. On the 11th day, the corneal endothelium developed again as a single layered structure on Descemet's membrane. It's seemed that corneal edema was induced as a result of severe damage corneal endothelium exposed to biochemical mediators such as prostaglandins released into the aqueous humor because the severity of corneal edema indicated some relation to changes in the concentration of prostaglandins in aqueous humor after anterior segmental ischemia.

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