Why is Intraocular Pressure Elevated in Chronic Simple Glaucoma?

Extracellular matrix in the trabecular meshwork

“…(Segawa 1979;Lütjen-Drecoll et al 1981;Rohen 1983;Lütjen-Drecoll et al 1986;Lütjen-Drecoll and Tamm 1987;Lutjen-Drecoll and Rohen 2001) The exact molecular nature of this material is not clear and a direct causal link to the increased outflow resistance has been difficult to establish. An additional caveat to these glaucoma studies is that, with few exceptions, (Rohen et al 1993) the tissue is from eyes that have been on various glaucoma medications for extended periods.…”

“…The figure is modified from several sources. (Tripathi 1971(Tripathi , 1977Grierson et al 1978;Rohen 1983;Grierson and Calthorpe 1989;Epstein and Rohen 1991;Maepea and Bill 1992;Lutjen-Drecoll 1999;Parc et al 2000) Fibronectin repeat type I, II and III domains, binding sites and alternative splicing. RGD, synergy and IDAPS sequences bind α5β1 and α4β1 integrins.…”

“…1). (Tripathi 1971;Inomata et al 1972;Tripathi 1977;Grierson et al 1978;Rohen 1983;Grierson and Calthorpe 1989;Epstein and Rohen 1991;Maepea and Bill 1992;Lutjen-Drecoll and Rohen 1994;Lütjen-Drecoll and Rohen 1996;Lutjen-Drecoll 1999;Parc et al 2000) These JCT cells form occasional contacts with each other, often via extended processes using gap and adherens junctions. (Inomata et al 1972;Grierson et al 1978) They also form similar junctions with SC inner wall endothelial cells.…”

Glaucoma model for stem cell transplantation research in New Zealand white rabbits

“…7 青光眼患者 (Leske, 2007)。原发性开角型青光眼(primary open angle glaucoma, POAG)是成年人青光眼中最常检出的一 类, 其发病进程通常伴随持续性眼压异常升高。目 前, 普遍认为 POAG 病人眼压升高是由于房水流出 通道中胞外基质(如纤维连接蛋白、粘多糖等)的异 常积聚引起房水循环受阻而导致 (Babizhayev & Brodskaya, 1989;Francois, 1975;Rohen, 1983 (Chihara, 1982), 因此不能对视野缺失进行根本性 治疗。随着干细胞研究的发展, 利用胚胎干细胞或 者神经干细胞载体移植, 通过其分化整合进而取代 缺失神经元的功能来修复中枢及周围神经系统的 损伤已经成为目前神经损伤性疾病的研究热点, 而 利用干细胞移植修复视网膜损伤也已成为了青光 眼研究的新方向 (Bull et al, 2008;Johnson et al, 2010)。 该方法需要一种能够模拟青光眼发病进程中 眼压处于长时期慢性升高, 进而导致视网膜神经节 细胞凋亡的动物模型; 且该模型眼球屈光间质清晰, 可对视网膜神经细胞缺失过程及干细胞整合替代 缺失神经细胞过程进行持续监测; 同时能够进行动 物视觉功能检测, 比如视网膜电图(electroretinogram, ERG)或者视觉诱发电位(visual evoke potential, VEP) 检测 (Ogata, 1971;Watts et al, 1989)来对比建模前后 及修复前后视觉功能的变化等要求。 新西兰白兔眼球特点明显、大小和结构类似人 眼、屈光间质清晰且病理变化易于检出, 是一种理 想的眼科疾病研究模式动物 (Bar-Ilan, 1984;Pierre V et al, 1977); 在青光眼研究中, 常被用于建立高 眼压模型以青光眼模拟病理进程, 研究发病机理及 降低眼压的方法 (Beitch & Eakins, 1969;Katz et al, 1975)。 早期的人及动物在体实验表明眼球经糖皮质 激 素 处 理 后 的 症 状 同 POAG 类 似 (Bill, 1977;Weinreb et al, 1985), 离体实验 表明糖皮质激素的主要作用部位是房水流出通道 中的小梁网状结构(trabecular meshwork, TM)。体外 培养经地塞米松处理的小梁网细胞表明, 其作用机 制主要表现在以下四个方面：1）改变小梁网处细 胞外基质的糖蛋白表达水平 (Steely et al, 1992;Yun et al, 1989); 2）通过影响肌动蛋白各亚基表达量来 影响细胞骨架结构的组织方式 (Clark et al, 1994) (Weinreb et al, 1985); Knepper 对兔眼使用地塞米松处理后, 青年 兔眼内压在给药后有轻微升高, 而老年兔眼压无显 著变化 (Knepper et al, 1978 …”

Non-penetrating intracanalicular partial trabeculectomy via the ostia of Schlemm's canal

“…However there is no such consensus about the localisation of the increased outflow resistance in POAG. A valuable review on this topic by Johnson and Johnson [31] indicate that trabecular meshwork is the site of abnormally increased outflow resistance in POAG, though histological examinations of the trabecular meshwork does not show specific abnormalities or ultrastructural changes, that could account for the abnormal IOP elevation [44,60].…”