Aqueous productionAqueous humour is produced from plasma by the ciliary epithelium of the ciliary body pars plicata, using a combination of active and passive secretion（既有主动分泌也有被动运输）.A high-protein filtrate passes out of fenestrated capillaries (ultrafiltration) into the stroma of the ciliary processes, from which active transport of solutes（溶质） occurs across the dual-layered ciliary epithelium. The osmotic gradient thereby established facilitates the passive flow of water into the posterior chamber. Secretion is subject to the influence of the sympathetic nervous system, with opposing actions mediated by beta-2 receptors (increased secretion) and alpha-2 receptors (decreased secretion)（互相拮抗调节）. Enzymatic action is also critical – carbonic anhydrase（碳酸酐酶） is among those playing a key role.[1]The trabecular meshwork（小梁网） (trabeculum) is a sieve-like（筛状） structure at the angle of the anterior chamber (AC) through which 90% of aqueous humour leaves the eye. It has three components.The uveal meshwork（葡萄网） is the innermost portion, consisting of cord-like（索状）endothelial cell-covered strands arising from the iris（虹膜） and ciliary body stroma. The intertrabecular（小梁） spaces are relatively large and offer little resistance to the passage of aqueous.The corneoscleral meshwork lies external to the uveal meshwork to form the thickest portion of the trabeculum. It is composed of layers of connective tissue strands with overlying endothelial-like cells. The intertrabecular spaces are smaller than those of the uveal meshwork, conferring greater resistance to flow.The juxtacanalicular (cribriform) meshwork is the outer part of the trabeculum, and links the corneoscleral meshwork with the endothelium of the inner wall of the canal of Schlemm. It consists of cells embedded in a dense extracellular matrix with narrow intercellular spaces, and offers the major proportion of normal resistance to aqueous outflow.The Schlemm canal is a circumferential channel within the perilimbal sclera. The inner wall is lined by irregular spindle-shaped endothelial cells containing infoldings (giant vacuoles) that are thought to convey aqueous via the formation of transcellular pores. The outer wall is lined by smooth flat cells and contains the openings of collector channels, which leave the canal at oblique angles and connect directly or indirectly with episcleral veins. Septa commonly divide the lumen into 2–4 channels.[1]Anatomy of outflow channels: A, Uveal meshwork; B, corneoscleral meshwork; C, Schwalbe line; D, Schlemm canal; E, connector channels; F, longitudinal muscle of the ciliary body; G, scleral spur Routes of aqueous outflow: A, trabecular; B, uveoscleral; C, irisAqueous Humor Drainage Pathways of Healthy and Glaucomatous EyesSimple intraocular pressure：High intraocular pressure has direct damage to the optic nerve. [2]High intraocular pressure directly oppresses optic nerve fibers, blocks axoplasmic transport, thereby damaging retinal ganglion cells. Increased intraocular pressure (IOP) causes stretching of the laminar beams and damage to retinal ganglion cell axons..[3, 4]Trans-lamina cribrosa pressure difference[5]Mitochondrial DNA mechanismAbnormally elevated intraocular pressure can directly lead to mtDNA damage and mutation, leading to mitochondrial dysfunction, thereby mtDNA further damages and mutates, forming a vicious circle, causing RGC progressive apoptosis.The vascular theory of glaucoma considers GON as a consequence of insufficient blood supply due to either increased IOP or other risk factors reducing ocular blood flow (OBF).Vascular dysregulation, rather than an atherosclerosis, leads to both low perfusion pressure and insufficient autoregulation. This in turn may lead to unstable ocular perfusion and thereby to ischemia and reperfusion damage.[6]High concentrations of glutamate causing RGC excitotoxic damage is the main cause of death in glaucoma patients.[7]Increased oxidative stress and increased ROS production play an important role in the development of glaucoma.[8]In recent years, it has been found that the immune system plays an important role in the development of GON.药物治疗的局限性：[9]1.很多患者仅用药物治疗不能降至理想的目标眼压。

2.药物副作用3.昂贵的药费4.长时间用药可能会影响今后的手术效果5.随着用药时间的延长，降眼压作用减弱6.可能与全身药物产生交叉反应7.药物产生的副作用干扰患者生活8.患者长期用药的依从性差Table 1 Summary of drugs used to treat glaucoma[10]LASER TREATMENT OF GLAUCOMALaser trabeculoplastySelective laser trabeculoplasty (SLT)Argon laser trabeculoplasty (ALT)Micropulse laser trabeculoplasty (MLT)Laser iridotomyDiode laser cycloablationLaser iridoplastyALT is effective as medical therapy in lowering IOP.The most common adverse eventwas a transient increase in IOP. The incidence of this event was 12% for an increase in IOP of .10 mm Hg and 34% for an increase in IOPof.5 mmHg. Other adverse events included a low-grade iritis.Complications• Bleeding occurs in around 50% but is usually mild and stops after only a few seconds; persiste nt bleeding can be terminated by increasing contact lens pressure.• IOP elevation. Usually early and transient but occasionally persistent.• Iritis. Especially if excessive laser is applied or post-laser steroid therapy is inadequate, or in darker irides (including those due to prostaglandin derivative treatment).• Corneal burns may occur if a contact lens is not used or if the AC is shallo w; these usually heal very rapidly without sequelae.• Cataract. Localized lens opacities occasionally develop at the treatment site; age-related cataract formation may be accelerated by iridotomy.TRABECULECTOMYNON-PENETRATING GLAUCOMA SURGERYDRAINAGE SHUNTS青光眼引流器的应用能减少结膜下和滤过道的瘢痕形成，从而大大提高手术的成功率。