HOYA Takuo Department of Ophthalmology. Shinshu University School of Medicine, 医学部附属病院眼科, 助手 (00201757)
MIYAZAKI Morito Department of Ophthalmology. Shinshu University School of Medicine, 医学部附属病院眼科, 助手 (90174169)
URAKAWA Yoshio Department of Ophthalmology. Shinshu University School of Medicine, 医学眼科学教室, 助手 (10160334)
西山 敬三 信州大学, 医学部眼科学教室, 助手 (90156125)
|Budget Amount *help
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 1988: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1987: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1986: ¥2,700,000 (Direct Cost: ¥2,700,000)
Human trabecular meshwork obtained from postmortem eyes was maintained in organ culture condition up to 12 weeks using solid agar method.
The effects of various agents upon human trabecular meshwork were studied using organ culture method as mentioned above. Various agents were as follows: (1) gold, (2) iron, (3) viscoelastic materials (methylcellulose (MC), sodium hyaluronate (SH) and chondroitin-6-sulfate (CDS)), (4) anti-glaucoma drugs (pilocarpine, epinephrine, -blockers (timolol, carteolol, befunolol)), (5) vitamin a, (6) vitamin C, (7) steroid (dexamethasone), and (8) photocoagulation.
Gold, iron, SH and CDS activated the trabecular cells to cause deposition of extracellular material. MC caused little change in trabecular meshwork cells and extracellular material.
Pilocarpine induced swelling of mitochondria, while epinephrine induced rounded cells and separation of cells from trabecular sheets. Beta-blockers induced accumulation of lysosome in cytoplasm.
A decrease of extracellular material and an increase of empty space occurred one day after addition of vitamin A, while an increase of extracellular material and a decrease of empty space one or two weeks after addition of vitamin C in the endothelial meshwork.
In a few cases an increase of extracellular material was observed, and in others no increase of extracellular material was observed two weeks after addition of dexamethasone. These results indicated that the former were steroid responders.
Photocoagulation on trabecular meshwork induced tissue defect and cell loss, and increased empty space in the endothelial meshwork.