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PubMed1986

Possible mechanisms underlying the differential effects of selective inhibitors of type A and type B monoamine oxidase on intraocular pressure in the cat.

Intraocular pressure and facility of aqueous outflow were measured in adult cats after topical application of clorgyline, a selective inhibitor of type A monoamine oxidase (MAO), or deprenyl, a selective inhibitor of type B of the enzyme. Clorgyline produced a dose-related lowering of intraocular pressure which was associated with a dose-related increase in outflow facility. Sympathetic denervation markedly reduced both these effects of clorgyline. Both effects, on the other hand, persisted after death of the animals. Deprenyl did not lower intraocular pressure; in fact, a tendency toward pressure elevation was apparent 2 hours after its administration. Outflow facility was not significantly changed. These results suggest that an endogenous substrate of type A MAO, presumably norepinephrine, is responsible for the ocular tension lowering effect of clorgyline. Because cessation of circulation after death did not abolish the effect, it is assumed that the trabecular meshwork is the site of action and that sympathetic innervation normally supplies an adrenergic neurotransmitter to the meshwork area. The tendency toward rise in intraocular pressure produced by deprenyl is probably due to alteration of aqueous humor formation rather than to a change in outflow resistance.

Animals↗
PubMed1995

Effects of cromakalim and nicorandil on intraocular pressure after topical administration in rabbit eyes.

In the study two potassium channel activators, cromakalim and nicorandil, were investigated in rabbits using three different levels of intraocular pressures (IOPs), including alpha-chymotrypsin-induced ocular hypertension, hypotension (IOP recovery method) and normal tension. Cromakalim significantly increased IOP during the initial period in normotensive and hypotensive rabbits, but in the later time, reduced IOP in the alpha-chymotrypsin-induced model. Nicorandil had a similar but less potent effect. In addition, cromakalim also affected ocular blood flows, which had a trend to reduce blood flow about 2-3 hr later, after topical administration of the eyedrop. Two possible mechanisms for increasing IOP effect of potassium channel activators were: (a) enhancing the formation of aqueous humor; (b) relaxing the trabecular meshwork to reduce the outflow of aqueous humor.

Administration, Topical↗
PubMed2000

Aqueous humor dynamics in monkeys with laser-induced glaucoma.

This study determines the effects of laser-induced glaucoma on aqueous humor dynamics of 18 cynomolgus monkeys. Baseline measurements of 12 monkeys included intraocular pressure (IOP) by pneumatonometry, aqueous flow by fluorophotometry and outflow facility by tonography. Beginning 4 to 14 days later, the trabecular meshwork of one eye was treated repeatedly with laser photocoagulation until elevated IOP was induced. Thirty-six to 75 days after the last laser treatment, all measurements were repeated. Between 1.7 and 11.4 years after laser treatment, the same 12 monkeys plus 6 additional monkeys underwent IOP and aqueous flow measurements. In addition, outflow facility was determined with fluorophotometry, and uveoscleral outflow was both calculated (n=18) and measured with an intracameral tracer (n=7). In glaucoma eyes compared to control eyes (n=12), IOP was increased (p<0.04) by at least 8 mmHg at Time 1 (1 to 3 months) or Time 2 (3 to 4 years) after laser treatment; aqueous flow was reduced (p=0.0007) by 46% at Time 1 but returned to baseline levels at Time 2; tonographic outflow facility was reduced (p=0.0008) by 71% at Time 1. In lasered eyes compared to control eyes, fluorophotometric outflow facility was reduced (p=0.0008; n=18) by 63%, and uveoscleral outflow was increased (p<0.05), whether calculated or measured with tracers at least 1 year after laser treatment. The increased IOP in monkeys with laser-induced glaucoma was caused by a sustained reduction in outflow facility. The uveoscleral outflow increase was not enough to prevent the rise in IOP.

Animals↗
PubMed2006

Preclinical pharmacology of AL-12182, a new ocular hypotensive 11-oxa prostaglandin analog.

PURPOSE: The aim of this study was to determine selected in vivo ocular properties of AL-12182 (5,6-dihydro-4,5-didehydro-11-deoxy-11-oxa-16-(3-chlorophenoxy)-omega-tetranor-PGF(2alpha) isopropyl ester) and the in vitro profile of its free acid, AL-12180. METHODS: Previously documented radioligand binding and functional assays involving human ciliary muscle cells (h-CM), human trabecular meshwork (h-TM) and other cells, and porcine ocular arteries were utilized. For in vivo procedures, we utilized rabbits, cats, and nonhuman primates to measure hyperemia, pupil diameter, and intraocular pressure (IOP), respectively. RESULTS: AL-12180 exhibited the highest affinity for the FP-receptor (K(i) = 143 +/- 36 nM) and much lower affinity for DP-, EP(3)-, IP-, and TP-receptors, and for several nonprostanoid receptors, enzymes, neurotransmitter uptake sites, ion channels, and other regulatory sites. AL-12180 activated phospholipase C-mediated phosphoinositide hydrolysis (potency, EC(50) = 13.7-42.7 nM) through the FP-receptor in a variety of cells, such as h-CM, h-TM cells, human embryonic kidney cells expressing the cloned human ciliary body FP-receptor (HEK-FP), mouse 3T3 cells, and rat vascular smooth muscle cells. AL-8810, an FP-antagonist, blocked the effects of AL-12180 in h-CM cells (IC(50) = 8.7 microM). AL-12180 also stimulated the mobilization of intracellular Ca(2+) ([Ca(2+)](i)) in h-TM cells (EC(50) = 111 +/- 36 nM), h-CM cells (EC(50) = 11 nM), and in host cells expressing the cloned human ciliary body FP-receptor (EC(50) = 5.9 +/- 3.1 nM). AL-12180 lacked significant agonist activity at DP-, EP(2)-, EP(4)-, IP-, and TP-receptors in cell-based assays. However, AL-12180 contracted porcine central retinal and short posterior ciliary arteries in vitro with micromolar potencies that appeared to involve TP-receptor activation. in vivo, AL-12182 elicited dose-related hyperemia in the rabbit eye, miosis in the cat eye, and ocular hypotension in the nonhuman primate eye. CONCLUSIONS: AL-12180 is a relatively potent and selective FP-receptor agonist whose isopropyl ester prodrug (AL-12182) lowers IOP by as much as 40% following topical ocular dosing in a laser-induced nonhuman primate model of ocular hypertension.

Animals↗
PubMed2002

Optimedin: a novel olfactomedin-related protein that interacts with myocilin.

Mutations in the MYOC gene may lead to juvenile open-angle glaucoma with high intraocular pressure, and are detected in about 4% of people with adult onset glaucoma. Most of these mutations are found in the third exon of the gene encoding the olfactomedin-like domain located at the C terminus of the protein. Another olfactomedin-related protein, known as noelin or pancortin, is involved in the generation of neural crest cells. Here we describe the identification of a novel olfactomedin-related gene, named optimedin, located on chromosome 1p21 in humans. Optimedin and noelin are both expressed in brain and retina. However, unlike noelin, rat optimedin is also highly expressed in the epithelial cells of the iris and the ciliary body in close proximity to the sites of Myoc expression. In the human eye, optimedin is expressed in the retina and the trabecular meshwork. Both optimedin and myocilin are localized in Golgi and are secreted proteins. The presence of mutant myocilin interferes with secretion of optimedin in transfected cells. Optimedin and myocilin interact with each other in vitro as judged by the GST pulldown, co-immunoprecipitation and far-western binding assays. The C-terminal olfactomedin domains are essential for interaction between optimedin and myocilin, while the N-terminal domains of both proteins are involved in the formation of protein homodimers. We suggest that optimedin may be a candidate gene for disorders involving the anterior segment of the eye and the retina.

Amino Acid Sequence↗
PubMed1995

Linkage of posterior polymorphous corneal dystrophy to 20q11.

Posterior polymorphous dystrophy (PPMD) is an autosomal dominant disorder of the cornea that is clinically recognized by the presence of vesicles on the endothelial surface of the cornea. The corneal endothelium is normally a single layer of cells that lose their mitotic potential after development is complete. In PPMD, the endothelium is often multi-layered and has several other characteristics of an epithelium including the presence of desmosomes, tonofilaments, and microvilli. These abnormal cells retain their ability to divide and extend onto the trabecular meshwork to cause glaucoma in up to 40% of cases. A large family with 21 members affected with PPMD was genotyped with short tandem repeat polymorphisms distributed across the autosomal genome. Linkage was established with markers on the long arm of chromosome 20. The highest observed LOD score was 5.54 (theta = 0) with marker D20S45. Analysis of recombination events in four affected individuals revealed that the disease gene lies within a 30cM interval between markers D20S98 and D20S108.

Chromosome Mapping↗
PubMed1997

Recent advances in molecular genetics of glaucomas.

Glaucomas are a heterogeneous group of eye conditions with manifestation from as early as birth to very late age of onset in life. The primary type of these conditions affecting children and juveniles are less frequent, but the prevalence of glaucomas affecting older people of > or = 70 years progressively rises to approximately 5%. The molecular genetics of three types of glaucoma have been the subject of investigation in the last few years. As a result, two loci (GLC3A and GLC3B) have been identified for primary congenital glaucoma, one locus (GLC1A) for juvenile-onset primary open angle glaucoma and a further two loci (GLC1B and GLC1C) for late-onset chronic open angle glaucoma. Early this year, the first set of mutations was described in the CYP1B1 (Cytochrome P4501B1) and TIGR (Trabecular meshwork Inducible Glucocorticoid Response Protein) genes for the GLC3A and GLC1A-linked families, respectively. The mapping of different types of glaucoma and mutation identification in these two genes are the focus of this review.

Adult↗
PubMed2000

Haploinsufficiency of the transcription factors FOXC1 and FOXC2 results in aberrant ocular development.

Anterior segment developmental disorders, including Axenfeld-Rieger anomaly (ARA), variably associate with harmfully elevated intraocular pressure (IOP), which causes glaucoma. Clinically observed dysgenesis does not correlate with IOP, however, and the etiology of glaucoma development is not understood. The forkhead transcription factor genes Foxc1 (formerly Mf1 ) and Foxc2 (formerly Mfh1 ) are expressed in the mesenchyme from which the ocular drainage structures derive. Mutations in the human homolog of Foxc1, FKHL7, cause dominant anterior segment defects and glaucoma in various families. We show that Foxc1 (+/-)mice have anterior segment abnormalities similar to those reported in human patients. These abnormalities include small or absent Schlemm's canal, aberrantly developed trabecular meshwork, iris hypoplasia, severely eccentric pupils and displaced Schwalbe's line. The penetrance of clinically obvious abnormalities varies with genetic background. In some affected eyes, collagen bundles were half normal diameter, or collagen and elastic tissue were very sparse. Thus, abnormalities in extracellular matrix synthesis or organization may contribute to development of the ocular phenotypes. Despite the abnormalities in ocular drainage structures in Foxc1 (+/-)mice, IOP was normal in almost all mice analyzed, on all genetic backgrounds and at all ages. Similar abnormalities were found in Foxc2 (+/-)mice, but no disease-associated mutations were identified in the human homolog FKHL14 in 32 ARA patients. Foxc1 (+/-)and Foxc2 (+/-)mice are useful models for studying anterior segment development and its anomalies, and may allow identification of genes that interact with Foxc1 and Foxc2 (or FKHL7 and FKHL14 ) to produce a phenotype with elevated IOP and glaucoma.

Animals↗
PubMed2005

Identification of a novel adult-onset primary open-angle glaucoma (POAG) gene on 5q22.1.

Glaucoma is a leading cause of blindness in virtually every country. Development of an accurate diagnostic test for presymptomatic detection of individuals at risk is an urgent requisition for this condition. Herein, we report mapping of a new adult-onset primary open-angle glaucoma (POAG) locus on 5q22.1 (GLC1G) and identification of its defective gene. Mutation screening of seven candidate genes from the GLC1G critical region (approximately 2 Mb between D5S1466 and D5S2051) identified only one significant alteration in the WDR36 (WD40-repeat 36) gene. This mutation (i.e. D658G) was segregated in all affected members of our first GLC1G-linked family but it was absent in 476 normal control chromosomes. Further screening of WDR36 in a total of 130 POAG families revealed 24 DNA variations. Overall, four mutations (N355S, A449T, R529Q and D658G) were identified in 17 (5.02-6.92%) unrelated POAG subjects, 11 with high-pressure and six with low-pressure glaucoma. These mutations were absent in a minimum of 200 normal control chromosomes and, further they were conserved between WDR36 orthologues in mouse, rat, dog, chimp and human. WDR36 is a novel gene with 23 exons, which encodes for 951 amino acids and a protein with multiple G-beta WD40 repeats. By northern blotting, two distinct mRNA transcripts of 5.9 and 2.5 kb were observed in human heart, placenta, liver, skeletal muscle, kidney and pancreas. WDR36 gene expression in lens, iris, sclera, ciliary muscles, ciliary body, trabecular meshwork, retina and optic nerve were established by RT-PCR. In mouse, two transcripts of 3.5 and 2.9 kb showed analogous expression patterns to human. mRNA expressions were detected in 7-, 11-, 15- and 17-day-old developing mouse embryos. In summary, WDR36 is a novel causative gene for adult-onset POAG at the GLC1G locus. Specific ocular expressions and observed mutations are consistent with WDR36 role in etiology of both high- and low-pressure glaucoma.

Amino Acid Substitution↗
PubMed2006

FGF19 is a target for FOXC1 regulation in ciliary body-derived cells.

The forkhead C1 (FOXC1) transcription factor is involved in the development and regulation of several organs, including the eye, where FOXC1 alterations cause iris, trabecular meshwork and corneal anomalies. Using nickel agarose chromatin enrichment with human anterior segment cells, we previously identified the fibroblast growth factor 19 (FGF19) locus as a gene potentially regulated by FOXC1. Here, we demonstrate that FGF19 is a direct target of FOXC1 in the eye. FOXC1 positively regulates FGF19 expression in corneal and periocular mesenchymal cells in cell culture and in zebrafish embryos. Through the FGFR4 tyrosine kinase, FGF19 promotes MAPK phosphorylation in the developing and mature cornea. During development, loss of either FOXC1 or FGF19 results in complementary, but distinct, anterior segment dysgeneses. This study reveals an important role for FOXC1 in the direct regulation of the FGF19-FGFR4-MAPK pathway to promote both the development and maintenance of anterior segment structures within the eye.

Animals↗
PubMed2003

Inhibition of 11beta-hydroxysteroid dehydrogenase type 1 lowers intraocular pressure in patients with ocular hypertension.

BACKGROUND: Intraocular pressure (IOP) is maintained by a balance between aqueous humour (AH) production (dependent on sodium transport across a ciliary epithelial bi-layer) and drainage (predominantly through the trabecular meshwork). In peripheral epithelial tissues, sodium and water transport is regulated by corticosteroids and the 11beta-hydroxysteroid dehydrogenase (11beta-HSD) isozymes (11beta-HSD1 activating cortisol from cortisone, 11beta-HSD2 inactivating cortisol to cortisone). AIM: To analyse expression of 11beta-HSD in the human eye and investigate its putative role in AH formation. DESIGN: Multipart prospective study, including a randomized controlled clinical trial. METHODS: The expression of 11beta-HSD1 in normal human anterior segments was evaluated by in situ hybridization (ISH). RT-PCR for 11beta-HSDs, glucocorticoid and mineralocorticoid receptors (GR, MR) was performed on human ciliary body tissue. AH cortisol and cortisone concentrations were measured by radioimmunoassay on specimens taken from patients with primary open-angle glaucoma (POAG) and age-matched controls. Randomized, placebo-controlled studies of healthy volunteers and patients with ocular hypertension (OHT, raised IOP but no optic neuropathy) assessed the effect of oral carbenoxolone (CBX, an inhibitor of 11beta-HSD) on IOP. RESULTS: ISH defined expression of 11beta-HSD1 in the ciliary epithelium, while RT-PCR analysis of ciliary body tissue confirmed expression of 11beta-HSD1, with additional GR and MR, but not 11beta-HSD2 expression. In both POAG patients and controls, AH concentrations of cortisol exceeded those of cortisone. The CBX-treated healthy volunteers who demonstrated the largest change in urinary cortisol metabolites, indicative of 11beta-HSD1 inhibition, had the greatest fall in IOP. Patients with OHT showed an overall reduction of IOP by 10% following CBX administration, compared to baseline (p<0.0001). DISCUSSION: CBX lowers IOP in patients with ocular hypertension. Our data suggest that this is mediated through inhibition of 11beta-HSD1 in the ciliary epithelium. Selective and topical inhibitors of 11beta-HSD1 could provide a novel treatment for patients with glaucoma.

11-beta-Hydroxysteroid Dehydrogenase Type 2↗
PubMed2002

VIP stimulation of cAMP production in corneal endothelial cells in tissue and organ cultures.

PURPOSE: To demonstrate that vasoactive intestinal peptide (VIP), an immunosuppressive factor found in the aqueous humor, is a modulator of the corneal endothelium (CE) stimulating its intracellular cAMP production. METHODS: Rabbit CE cells in cell culture and CE cells in cornea cup organ cultures established from bovine and human donor eyes were treated with VIP at varying concentrations (0, 10(-11)-10(-6) mol/L) for a constant time (4 minutes) or varying times (1, 3.25, 10, 15 minutes) at a constant concentration (1 x 10(-6) mol/L). Intracellular cAMP was extracted and its concentrations were determined by radioimmunoassay. Agonists that are known to modulate the intracellular cAMP concentrations of target cells were allowed to react with cultured rabbit CE cells at 1 x 10(-6) mol/L for 4 minutes. RESULTS: Vasoactive intestinal peptide stimulated the intracellular cAMP production in CE cells in a dose- and time-dependent manner. At concentrations lower than 10(-9) mol/L, VIP showed little effect. Treatment with 10(-8), 10(-7), and 10(-6) mol/L VIP for 4 minutes, however, increased the intracellular cAMP by 5.7-, 12.3-, and 9.5-fold, respectively, compared with the basal level in rabbit CE cell cultures, and by 19.5-, 38.7-, and 23.3-fold, respectively, in CE cells in bovine cornea cups. The effect of VIP was confirmed in two pairs of donor human corneas in which an average of 2.7-fold stimulation by 5 x 10(-7) mol/L was observed. Treatment of rabbit CE cells with 1 x 10(-6) mol//L VIP for 1 to 15 minutes elevated the intracellular cAMP level by six- to 69-fold. Among the agonists tested, alpha-melanocyte-stimulating hormone and glucagon were not effective, whereas l-isoproterenol and prostaglandin E1 were capable of stimulating the intracellular cAMP levels in rabbit CE cells. CONCLUSIONS: The current study demonstrated that VIP stimulated cAMP production in CE cells, similar to that shown previously in trabecular meshwork and nonpigmented ciliary epithelial cells. Tissues bathed in the aqueous humor are thus responsive to VIP modulation.

Aged↗
PubMed1993

The Glenn A. Fry Award Lecture 1992: aqueous humor proteins: a key for unlocking glaucoma?

In this report I summarize recently reported studies which establish the existence of a previously undocumented diffusional pathway for plasma-derived proteins from the ciliary body stroma to the anterior chamber of the normal mammalian eye via the iris root. The data support the hypothesis that nearly all of the plasma-derived protein present in the aqueous humor of the anterior chamber arrives via this pathway, thus by-passing the posterior chamber. Additional studies suggest that some of the protein transported via the pathway is shunted directly into the trabecular meshwork and aqueous outflow pathways. Perfusion studies show how the perfused eyes were later immunohistochemically stained to reveal the distribution and qualitative amounts of serum albumin. These studies strongly suggest that the well-known "wash-out" effect, encountered in experimental studies of aqueous outflow, arises predominantly from wash-out of the protein depot that serves as the anterior diffusional pathway for proteins. Taken as a whole, these studies support the hypothesis that protein is a physiologically relevant and important element in the generation of normal aqueous outflow resistance, possibly more important than glycosaminoglycans (GAG's).

Animals↗
PubMed1996

Rubeosis of the iris in proliferative vitreoretinopathy.

PURPOSE: The authors report the findings and clinical course of rubeosis in patients with essentially reattached retinas after vitrectomy and silicone oil for proliferative vitreoretinopathy (PVR). METHODS: From 1989 on, the authors prospectively noted all patients with rubeosis and with attached retina posterior to the buckle after vitrectomy and silicone oil for PVR as a complication of rhegmatogenous retinal detachment. RESULTS: Thirty-eight patients (38 eyes) were studied. Mean follow-up after the appearance of rubeosis was 27 months (range, 6-66 months) in all patients, peripheral residual retinal detachment coexisted with rubeosis. Hypotony occurred in six patients. Cyclocryocoagulation for neovascular glaucoma had been performed in four patients. The peripheral detached retina was removed in 16 patients, resulting in total disappearance of rubeosis in 7 patients and regression in 4 more patients. In patients with visible, nonradially oriented iris vessels, the authors found vessels in the anterior chamber angle crossing the trabecular meshwork. The frequently present anterior synechiae in association with vessels never totalled more than three clock hours (except in the four patients who underwent cyclocryocoagulation). CONCLUSIONS: Detached retina peripheral to dense photocoagulation scars was present in all of these patients. Removal of this peripheral detached retina was statistically significantly associated with disappearance of rubeosis, which suggests that the peripheral detachment was a causative factor. Extensive anterior synechiae are not formed frequently in this condition. This may explain the infrequent (11%) occurrence of neovascular glaucoma. However, hypotony is more frequent.

Fluorescein Angiography↗
PubMed2000

Intraocular melanoma spread to regional lymph nodes: report of two cases.

PURPOSE: To report two cases of regional lymphatic spread of primary uveal melanoma. METHODS: The clinical records of two patients who underwent enucleation for uveal melanoma and later developed regional lymph node metastases were reviewed. One of the two eyes was initially treated with proton beam irradiation. Histologic sections of the enucleated eyes and excised lymph nodes were examined. RESULTS: The melanomas arose in the choroid and ciliary body of the two patients and spread to regional lymph nodes 2 years after enucleation. The choroidal melanoma recurred after irradiation, diffusely infiltrated the uveal tract, and extended into the conjunctiva via an emissary canal. The ciliary body melanoma spread through the trabecular meshwork to the conjunctiva. CONCLUSIONS: Choroidal and ciliary body melanoma may rarely exhibit regional lymph node metastasis. This mode of metastasis may occur after extraocular spread and invasion of conjunctival lymphatics.

Adult↗
PubMed1998

Diagnosis and management of pigmentary glaucoma.

Pigment dispersion syndrome and pigmentary glaucoma affect typically young, myopic persons. Iridozonular contact causes pigment dispersion and obstruction of the trabecular meshwork. Accumulation of pigment may result in transient elevation of intraocular pressure or irreparable damage to the meshwork accompanied by uncontrolled glaucoma. In the reviewed publications the transition from pigment dispersion syndrome to pigmentary glaucoma was found to be 20%. The main risk factors for the transition were ocular hypertension and myopia. Dapiprazole, an alpha-adrenergic blocking agent, was found to be effective in treating pigmentary glaucoma and in preventing pressure spikes after exercise. Dapiprazole causes miosis without affecting accommodation. Yttrium aluminum garnet laser iridotomy reduced the incidence of ocular hypertension in pigment dispersion syndrome, although the effect was less pronounced in persons older than 40 years of age. Lattice degeneration was found in 33.3% of the eyes with pigment dispersion syndrome.

Adrenergic alpha-Antagonists↗
PubMed1998

The psychology of the glaucoma patient.

Under physiological conditions, intraocular pressure (IOP) is controlled by the autonomic and central nervous systems. Correspondingly, nerve fibers and neurotransmitters are present in ciliary body and trabecular meshwork. IOP responds to physical as well as psychological stimuli in healthy individuals. In patients with dysregulated IOP, e.g., in those with primary open-angle glaucoma, emotional instability without a specific personality pattern could be found. Whereas the statistical association between emotional changes and glaucoma is obvious, the causal relationship remains to be clarified. It is at least plausible that psychic stress may have an influence on IOP. However, the sequence of the events is unknown (emotional disturbance can be the result of the disease or it can be a primary sign of a nervous dysfunction). Therefore, it seems meaningful--in addition to standard glaucoma therapy--to try to improve the patient's emotional condition, both for treatment of the glaucoma and for the patient's general quality of life.

Exercise↗
PubMed2000

Nonpenetrating filtering surgery in glaucoma.

Since 1967, trabeculectomy has been the standard drainage operation for most cases of medically uncontrolled glaucoma. It is associated with significant risk of hypotony, hyphema, choroidal effusion or hemorrhage, and bleb failure. Toward the goal of a safer and more reproducible glaucoma filtering surgery, nonperforating filtering surgeries are now performed in primary open-angle glaucoma, normal-pressure glaucoma, and most cases of secondary glaucoma. The site of highest resistance to outflow, the juxtacanalicular trabecular meshwork, is bypassed with avoidance of penetration into the anterior chamber. Different techniques of nonpenetrating filtering surgeries are discussed here.

Anterior Chamber↗