Czepita Damian
Z Katedry i Kliniki Okulistyki Pomorskiej Akademii Medycznej al. Powstańców Wlkp. 72, 70-111 Szczecin.
Ann Acad Med Stetin. 2005;51(1):27-31.
The aim of this paper is to present and discuss the contemporary possibilities and perspectives of applying neuroprotective mechanisms in the treatment of glaucoma.
A review of the newest concepts concerning neuroprotective action of antiglaucoma drugs was done.
Not until recently was it believed that glaucoma is caused by an increased intraocular pressure. When it comes to diagnosing glaucoma it is nowadays considered that intraocular pressure is not the most important factor. Glaucoma is presently regarded as a condition in which characteristic changes in the appearance of the optic disc and distinctive progressive changes in the visual field occur because of progressive and irreversible destruction of the retinal ganglion cells. Intraocular pressure may sometimes, but not necessarily, accompany those changes. Hence, it is thought that neuroprotection in glaucoma is aimed at delaying or blocking the mechanisms of ganglion cell degeneration. Two groups of antiglaucoma drugs with neuroprotective action can be distinguished, depending on whether neroprotective action is direct or indirect. Drugs with direct neuroprotective action are more effective at preventing changes created by glaucoma. However, the majority of antiglaucoma drugs act indirectly. Sympatholytics, carbonic anhydrase inhibitors, analogs of prostaglandins, parasympathicomimetics, sympathicomimetics as well as hyperosmotic agents lower intraocular pressure and lead to an increase in blood flow through vessels of the retina and optic nerve. Therefore, almost all antiglaucoma drugs in an indirect way delay the process of gradual and irreversible degeneration of retinal ganglion cells. Only a few antiglaucoma drugs show direct neuroprotective action, among them betaxolol, metipranolol, brimonidine and clonidine. Additionally, calcium-channel blockers are generally administered in the treatment of glaucoma. One may anticipate that newer and more effective antiglaucoma drugs will be available in future. Possibly, mechanisms of direct neuroprotection will be exploited in their design. Glaucoma treatment may be based on NMDA, AMPA, kainate or metabotropic antagonists. Moreover, nitric oxide inhibitors, growth factors, neurotrophins, gangliosides or antioxidants emerge as candidate antiglaucoma drugs.
本文旨在介绍和讨论应用神经保护机制治疗青光眼的当代可能性和前景。
对有关抗青光眼药物神经保护作用的最新概念进行了综述。
直到最近人们还认为青光眼是由眼内压升高引起的。在青光眼的诊断方面，如今认为眼内压并非最重要的因素。目前青光眼被视为一种由于视网膜神经节细胞进行性和不可逆性破坏，导致视盘外观出现特征性变化以及视野发生明显进行性变化的病症。眼内压有时可能伴随这些变化，但并非必然。因此，人们认为青光眼的神经保护旨在延缓或阻断神经节细胞变性的机制。根据神经保护作用是直接还是间接的，可以区分出两组具有神经保护作用的抗青光眼药物。具有直接神经保护作用的药物在预防青光眼所致变化方面更有效。然而，大多数抗青光眼药物起间接作用。抗交感神经药、碳酸酐酶抑制剂、前列腺素类似物、拟副交感神经药、拟交感神经药以及高渗剂可降低眼内压，并导致视网膜和视神经血管的血流量增加。因此，几乎所有抗青光眼药物都以间接方式延缓视网膜神经节细胞逐渐不可逆变性的过程。只有少数抗青光眼药物具有直接神经保护作用，其中包括倍他洛尔、美替洛尔、溴莫尼定和可乐定。此外，钙通道阻滞剂通常用于青光眼的治疗。可以预期未来会有更新、更有效的抗青光眼药物。可能在其设计中会利用直接神经保护机制。青光眼治疗可能基于N-甲基-D-天冬氨酸（NMDA）、α-氨基-3-羟基-5-甲基-4-异恶唑丙酸（AMPA）、海人藻酸或促代谢型拮抗剂。此外，一氧化氮抑制剂、生长因子、神经营养因子、神经节苷脂或抗氧化剂也成为抗青光眼药物的候选者。
