Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Trabecular Meshwork”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 955 records · Page 53Linked to original sources
PubMed1986

[Pseudoexfoliation syndrome as a cause of chronic glaucoma].

A clinical study of 70 ambulant and stationary patients showed that of 104 eyes with pseudoexfoliation (PE) syndrome there were 62 eyes (60%) with confirmed chronic glaucoma and 8 (8%) with suspected chronic glaucoma. This is a considerably higher percentage than would normally be expected in a comparable group with an average age of 75 years (between 50 and 95 years). The biomicroscopic picture reveals symptoms of dispersion glaucoma with pigment participation. Provoked through diagnostic mydriasis by means of 0.5% tropicamide HCl and 10% phenylephrine HCl, 44 (52%) of the 84 eyes tested showed a significant increase in intraocular pressure by greater than or equal to 4 mm Hg and 20 (24%) by greater than or equal to 10 mm Hg. A possible cause of the pressure increase, in each case with open chamber angle, is the observed dispersion of the PE material and the adhering pigment fragments. From this observation and from a comparison with existing literature, it is inferred that the PE layers are the result of a sedimentation which also takes place in the chamber angle and in the trabecular meshwork, causing, in a first stage, chronic secondary open-angle glaucoma. In a second stage, the sediments may become detached from their base and cause pressure peaks through acute obliteration of the trabecular meshwork. The lack of proof of an inflammatory, immunological, or hereditary origin of this disease where it frequently occurs in certain areas, leads to the hypothesis of an alimentary or toxic disorder.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed2000

A Case Report of Neovascular Glaucoma Due to Carotid Artery Occlusive Disease. Diagnosis of Neovascular Glaucoma and Histological Characteristics.

Purpose: The methods of diagnosing neovascular glaucoma were evaluated in a case with carotid artery occlusive disease. A trabeculectomy specimen taken from this patient was examined histologically to find the characteristic picture of this slowly progressive neovascular glaucoma.Materials and Methods: The left eye of a 48-year old man with neovascular glaucoma due to carotid artery occlusive disease had been previously diagnosed as uveitis with ocular hypertension. His left eye was examined by fluorescein fundus and gonioangiography. Trabeculectomy was performed because of uncontrolled intraocular pressure and the trabeculectomy specimen was examined histologically including immunohistochemistry with antibodies against von Willebrand factor antigen.Results: The characteristic picture of fluorescein fundus angiography was filling delay in the choroid and stained walls of the retinal arteries and veins. Fluorescein gonioangiography using a fundus camera clearly demonstrated new vessels in the pupil and angle with intense fluorescein leak in spite of faint neovascularization in those areas when observed by slit lamp with gonioscopy. Histological examination of the trabeculectomy specimen revealed proliferation of new vessels in the spaces of the trabecular meshwork and focal occlusion of Schlemm's canal.Conclusion: Fluorescein fundus angiography and gonioangiography by fundus camera is very useful for diagnosis of neovascular glaucoma due to carotid artery occlusive disease. Neovascular proliferation in the trabecular meshwork with slight of peripheral anterior synechia and focal occlusion of Schlemm's canal may be peculiar to such slowly progressive neovascular glaucoma.

Journal Article↗
PubMed1989

Comparative study of argon laser trabeculoplasty in primary open-angle and pseudoexfoliation glaucoma.

In 93 phakic eyes--52 eyes with primary open-angle and 41 eyes with exfoliation glaucoma--with increased intraocular pressure, argon laser trabeculoplasty was performed. Fifty to sixty burns were made over 180 degrees of the lower trabecular meshwork. During the follow-up period, visual acuity, intraocular pressure, medication changes and the need for surgery were studied. In 25 eyes a second laser treatment was performed over 180 degrees of the upper trabecular meshwork. Intraocular pressure control was obtained in 81% of the eyes with primary open-angel glaucoma and 71% of the eyes with pseudoexfoliation glaucoma. The average reduction of pressure obtained after laser trabeculoplasty was 9.22 mm Hg for the group of eyes with primary open-angle glaucoma and 13.42 mm Hg for the group of eyes with pseudoexfoliation glaucoma (p less than 0.001). Reduction in medical treatment was obtained in 27 eyes from the 71 eyes with successful reduction of the intraocular pressure. In 6 eyes with successful results after argon laser trabeculoplasty, cataract extraction was performed. The intraocular pressure remained normal in all eyes after the operation.

Aged↗
PubMed2000

[A case report of neovascular glaucoma due to carotid artery occlusive disease--diagnosis of neovascular glaucoma and histological characteristics].

PURPOSE: The methods of diagnosing neovascular glaucoma were evaluated in a case with carotid artery occlusive disease. A trabeculectomy specimen taken from this patient was examined histologically to find the characteristic picture of this slowly progressive neovascular glaucoma. MATERIALS AND METHODS: The left eye of a 48-year old man with neovascular glaucoma due to carotid artery occlusive disease had been previously diagnosed as uveitis with ocular hypertension. His left eye was examined by fluorescein fundus and gonioangiography. Trabeculectomy was performed because of uncontrolled intraocular pressure and the trabeculectomy specimen was examined histologically including immunohistochemistry with antibodies against von Willebrand factor antigen. RESULTS: The characteristic picture of fluorescein fundus angiography was filling delay in the choroid and stained walls of the retinal arteries and veins. Fluorescein gonioangiography using a fundus camera clearly demonstrated new vessels in the pupil and angle with intense fluorescein leak in spite of faint neovascularization in those areas when observed by slit lamp with gonioscopy. Histological examination of the trabeculectomy specimen revealed proliferation of new vessels in the spaces of the trabecular meshwork and focal occlusion of Schlemm's canal. CONCLUSION: Fluorescein fundus angiography and gonioangiography by fundus camera is very useful for diagnosis of neovascular glaucoma due to carotid artery occlusive disease. Neovascular proliferation in the trabecular meshwork with slight of peripheral anterior synechia and focal occlusion of Schlemm's canal may be peculiar to such slowly progressive neovascular glaucoma.

Carotid Stenosis↗
PubMed1999

Histopathological changes in iridocorneal angle of inherited glaucoma in rabbits.

BACKGROUND: We examined morphologically the angular region of eyes affected by inherited glaucoma in rabbits genetically developed by crossbreeding in order to investigate the etiologic changes in the iridocorneal angle and to establish whether this strain of rabbit is a suitable animal model of goniodysgenetic glaucoma in humans. METHODS: The angular regions of both normal and glaucomatous eyes from four rabbits having unilateral inherited glaucoma were observed with light and electron microscopy. RESULTS: In the glaucomatous eyes angular region, the aqueous plexus corresponding to Schlemm's canal in humans was open and located far peripherally to the peripheral margin of the anterior chamber angle, although the plexus of one glaucomatous eye was poorly developed with a small lumen. In the angular meshwork, which corresponds to the trabecular meshwork in humans, a thick abnormal tissue with round cells embedded in the extracellular matrix was located just beneath the plexus. A large amount of extracellular matrix of basal lamina-like material was observed in the thick tissue. In the normal eyes, the angular region consisted of well-developed trabecular sheets with neither a thick tissue nor accumulations of extracellular matrix in the angular meshwork. CONCLUSION: The findings observed in the glaucomatous eyes are much the same as those observed in goniodysgenetic glaucoma in humans, suggesting that this strain of inherited glaucoma rabbits is a suitable animal model of goniodysgenetic glaucoma in humans. The present study also supports the hypothesis that the presence of a thick subcanalicular tissue due to maldevelopment of the iridocorneal angle is one of the main causes of this type of glaucoma.

Animals↗
PubMed2006

Myocilin-associated exosomes in human ocular samples.

Mutations in myocilin result in ocular hypertension, likely due to decreased drainage of aqueous humor through the trabecular meshwork. Since less myocilin is found in the aqueous humor of those with disease-causing mutations, understanding myocilin's role in the aqueous humor is of clinical importance. Recently, myocilin was shown to exit cultured trabecular meshwork cells in association with shed vesicles called exosomes. To examine relevance of this finding in a physiological setting, the present study examined three different types of ocular samples for the presence of myocilin-associated exosomes. Using differential centrifugation steps, we found myocilin associated with exosomes isolated from effluent collected from human anterior segments in organ culture and aqueous humor obtained from human cadaveric eyes or from patients undergoing excisional surgery. Similar to results with cultured cells, myocilin associated predominately with exosomes in fresh samples, appeared mostly soluble at later times, and had biochemical properties (density of 1.13-1.19 g/ml in linear sucrose gradient) similar to those characteristics of exosomes. These data indicate that exosomes are present and may facilitate the transport of myocilin into the extracellular space of human ocular cells.

Aqueous Humor↗
PubMed1992

[Primary open angle glaucoma and low tension glaucoma--pathogenesis and mechanism of optic nerve damage].

The etiology, pathogenesis and mechanism of optic nerve damage in primary open angle glaucoma (POAG) and low tension glaucoma (LTG) were investigated by experimental glaucoma in monkey and by follow-up studies of many patients over 15 years, by pathohistological and immunohistochemical analysis. 1) LTG was proved to be a real glaucoma, showing pressure-dependent optic nerve damage. The pathological entity was a primary weakness of the lamina cribrosa (LC), and therefore even normal pressure could deform the LC. Due to backward distortion of LC the channels were disarranged and twisted, inducing mechanical optic nerve damage. There was no active vascular damage or vascular constriction at the site of the optic nerve damage. The filling defects of the advanced glaucomatous optic disc were not the cause of optic nerve damage, but the result of regressive vascular change after axon bundle loss. Splinter hemorrhage of the optic disc might be the result of the same process. 2) The weakness of LC might be induced by the abnormal metabolism of the extracellular matrix of the LC. 3) To arrest the progressive optic nerve damage in LTG, the intraocular pressure (IOP) should be maintained under 12, or ideally, 10 mmHg. 4) The optic nerve damage in POAG was not only pressure-dependent, but also dependent on the weakness of the LC, as in the case of LTG. In the early stage the IOP should be under 19 mmHg, in the advanced stage under 14 mmHg in order to arrest progression for over 15 years. 5) In advanced experimental glaucoma of monkeys, the LC showed reduction of elastin, fragmentation of collagen, and change of proteoglycans. 6) As in the LC, the trabecular meshwork also showed abnormal metabolism and abnormal deposits on the extracellular matrix in POAG, and LTG as well. 7) POAG and LTG might belong to the same family in which common abnormal metabolism of LC and trabecular meshwork induce various clinical features.

Adolescent↗
PubMed1976

[Phacolytic and hemolytic glaucoma (author's transl)].

Clinical and histological data of four patients with acute secondary open-angle glaucoma are described. These included two hemolytic and one phacolytic glaucoma. Another patient showed a transition of hemolytic to a hemosiderotic glaucoma. The hemolytic glaucoma follows a hemorrhage of the vitreous, it is characterised by an open-angle with red-brown pigment deposits on the trabecular meshwork. Macrophages can be isolated from the aqueous humor by zentrifugation. The same macrophages and fragments of lysed red blood cells are histologically visible in the vitreous as well as in the anterior chamber and the trabecular meshwork. The cause of the large vitreous hemorrhage is often a retinal detachment. The hemolytic glaucoma must be clearly distinguished from hemosiderotic and neovascular glaucoma. A transition from hemolytic to hemosiderotic glaucoma is possible. The simultaneous description of hemolytic and phacolytic glaucoma follows by reason of the same pathogenetic mechanism. The treatment of hemolytic glaucoma follows the standard medical therapy of glaucoma. If this therapy will be unsuccessful, a paracentesis with irrigation of the anterior chamber may be required. The only therapy of phacolytic glaucoma is immediate intracapsular cataract extraction.

Aged↗
PubMed1995

Endothelin subtypes: effect on isolated rhesus monkey ciliary muscle.

The effects of endothelin (ET)-1, ET-2, ET-3 and sarafotoxin S6C on the contractile response in the longitudinal and coronal vectors of the isolated rhesus monkey ciliary muscle were studied. Fresh ciliary muscle strips from young and middleaged rhesus monkeys were mounted in an apparatus capable of monitoring contractile force simultaneously in the two vectors. The responses to the ET compounds were measured and compared to those produced with 1 microM carbachol. ET-1 produced contractions of up to 15% of the near-maximum response to carbachol in both vectors of 66% of ciliary muscle strips studied. In responsive strips, the maximal ET-1 induced contraction was approximately equal in both vectors, but the longitudinal vector was approximately 5-fold more sensitive than the circular. All ciliary muscle strips responded reproducibly to carbachol. None of the other ET compounds tested had any effect, suggesting that the ETA receptor may predominate in rhesus monkey ciliary muscle. Because ET-1 induces only weak and interindividually variable contraction in isolated rhesus monkey ciliary muscle strips, ET-1's enhancement of outflow facility with only minimal induction of accommodation in the living monkey may be due to effects directly on the trabecular meshwork. However, the 5-fold greater potency of ET-1 in the longitudinal compared to the circular contractile vector may indicate that selective contraction of the longitudinal portion of the ciliary muscle with consequent deformation of the trabecular meshwork but not the lens is also involved.

Animals↗
PubMed1975

Hemolytic glaucoma.

The clinical manifestations of hemolytic glaucoma in five patients showed that the glaucoma began after a large intraocular hemorrhage. Gonioscopy revealed open angles in the anterior chamber and reddish-brown pigment covering the trabecular meshwork. Numerous red-tinted blood cells were floating in the aqueous humor; some of these were macrophages found by cytologic examination to contain golden-brown pigment granules. The presumed cause of hemolytic glaucoma is obstruction of the trabecular meshwork by fragments of hemolyzed red blood cells and hemoglobin-laden macrophages. Two patients, whose intraocular pressures were not decreased with medication, improved remarkably after irrigation of hemolytic debris from the anterior chamber.

Acetazolamide↗
PubMed2002

Selective laser trabeculoplasty: a new treatment option for open angle glaucoma.

Selective laser trabeculoplasty (SLT) is a safe and effective treatment modality for lowering the intraocular pressure in patients with open angle glaucoma. The preservation of the trabecular meshwork architecture and the demonstrated efficacy in lowering intraocular pressure makes the SLT a reasonable and safe alternative to argon laser trabeculoplasty. In addition, SLT is a potentially repeatable procedure because of the lack of coagulation damage to the trabecular meshwork and the demonstrated efficacy in patients with previously failed argon laser trabeculoplasty treatment. Furthermore, SLT can be considered as a primary treatment option in patients who cannot tolerate or are noncompliant with their glaucoma medications, while not interfering with the success of future surgery. Due to its nondestructive properties and low complication rate, SLT has the potential to evolve as an ideal first-line treatment in open angle glaucoma.

Glaucoma, Open-Angle↗
PubMedDate not supplied

Effect of particle size of polymeric nanospheres on intravitreal kinetics.

In this study, we injected nanospheres containing a fluorescein derivative into the vitreous cavity of pigmented rabbit eyes and evaluated their intraocular kinetics as drug carriers in vivo. Polystyrene nanospheres (2 microm, 200 nm and 50 nm in diameter) containing a fluorescein derivative were used in this study. A suspension of each particle was prepared by diluting with distilled water at a concentration of 10 microg/ml equivalent to sodium fluorescein. The suspension of nanospheres was injected once into the vitreous cavity of unilateral eyes of pigmented rabbits. A sodium fluorescein solution of the same concentration was injected once into the vitreous cavity of the other eye as the control. The intraocular kinetics of nanospheres was evaluated by measuring vitreous fluorescence using a scanning fluorophotometer. To investigate elimination pathways of nanospheres in detail, serial cross-sections of the eyes were examined with a fluorescence microscope. The fluorescence derived from nanospheres was observed in the vitreous cavity for over 1 month (2 microm: t(1/2) = 5.4 +/- 0.8 days, 200 nm: t(1/2) = 8.6 +/- 0.7 days, 50 nm: t(1/2) = 10.1 +/- 1.8 days), whereas that in the control eyes completely disappeared within 3 days (t(1/2) = 7.8 +/- 0.7 h). The elimination half-life from the vitreous cavity correlated well with the particle diameter (r = -0.997, p = 0.007). Histological studies using a fluorescence microscope revealed that nanospheres with a diameter of 2 microm were seen in the vitreous cavity and trabecular meshwork, while nanospheres with a diameter of smaller than 200 nm were also observed in the retina as well as these tissues. Our findings indicated that nanospheres may be beneficial as a drug carrier to the retina, vitreous and trabecular meshwork.

Animals↗
PubMed1985

Intraorbital cerebrospinal fluid outflow and the posterior uveal compartment of the hamster eye.

An ultrastructural and tracer study was undertaken to determine normal outflow pathways of cerebrospinal fluid (CSF) at the terminal subarachnoid space (SAS) of the optic nerve. In the morphological studies, the optic nerve dura and arachnoid were found to be continuous with the sclera of the eye beyond the optic nerve SAS. The pia mater is continuous with the inner sclera and the lamina fusca of the eye. Montages and serial sections demonstrated that the distal SAS is divided into numerous tortuous channels to form an "arachnoidal trabecular meshwork". Spaces of this meshwork continue into "microcanals" which bypass the outer arachnoid barrier layers of the optic nerve meninges to reach the sclera and posterior intraorbital connective tissue. Ferritin infused into the cisterna magna entered the optic nerve SAS within 1 min and reached arachnoidal trabecular meshwork channels and the microcanals within 8 min. It then passed into intraorbital connective tissue spaces at the posterior pole of the eye. Ferritin appeared to be blocked by the lamina fusca and a newly discovered "posterior compact zone" which together prevented its entrance into the choroidal interstitium. These observations suggest that a "subarachnoidal-scleral-orbital outflow pathway" provides a route for CSF drainage from the optic nerve SAS to intraorbital connective tissue. The previously described "posterior uveal compartment" in the hamster eye (Kelly et al. 1983) appears to be relatively isolated from this subarachnoidal-scleral-orbital CSF outflow.

Animals↗
PubMed1997

Mechanisms of acute intraocular pressure increases after phacoemulsification lens extraction in dogs.

OBJECTIVE: To investigate the mechanisms by which intraocular pressure (IOP) increases acutely after phacoemulsification (PE) lens extraction in clinically normal dogs. ANIMALS: 24 young adult dogs. PROCEDURE: Intraocular pressure was monitored for up to 24 hours after unilateral intercapsular PE in 17 clinically normal, adult dogs. In 8 of these dogs, use of 2% hydroxypropyl methylcellulose (HPMC) aided capsulorhexis. Mean volume of irrigation, PE time, and power were constant between groups. After surgery, dogs were randomized then euthanatized, and eyes were examined grossly and histologically at 0 (n = 4), 3 (n = 7), and 24 hours (n = 6) after PE. Seven additional dogs underwent anterior chamber decompression alone (n = 4) or served as morphologic controls (n = 3). RESULTS: Intraocular pressure peaked by postoperative hour 3 at 49.9 +/- 5.0 mm of Hg and normalized by 24 hours. Use of HPMC did not affect the peak or duration of IOP increase. Blood refluxed into the collecting channels and corneoscleral trabecular meshwork in operated eyes. Computer-aided morphologic analysis indicated significant (P < 0.001) reduction in ciliary cleft cross-sectional surface area and width immediately after PE, but not after anterior chamber decompression alone. Cleft collapse was significantly (P < 0.02) greater at 24 than at 3 hours, despite return of IOP to control values by 24 hours. Plasmoid aqueous also was found in the meshwork. CONCLUSIONS AND CLINICAL RELEVANCE: Sudden, large increases in IOP with few overt clinical signs may occur immediately after lens extraction in dogs. Such increases risk compromising the corneal incision and may damage the optic nerve, thereby complicating lens extraction. Structural alterations in the trabecular meshwork persist after IOP has normalized in 24 hours and may contribute to genesis of glaucoma in the late postoperative period.

Analysis of Variance↗
PubMed1976

Ghost cells as a cause of glaucoma.

Clinical and investigative evidence indicated a glaucoma caused mainly by degenerated red blood cells, or ghost cells. These ghost cells, with altered shape, color, and pliability, accumulated in the vitreous cavity after hemorrhage. Following disruption of the anterior hyaloid face, they passed into the anterior chamber and caused severe glaucoma. In the anterior chamber, the tiny, khakicolored cells, circulating slowly, were frequently mistaken for white blood cells. They covered the trabecular meshwork or filled the inferior angle with a pathognomonic khaki-colored layer. They were identified by phase-contrast microscopic examination of anterior chamber aspirates. The decreased pliability of these degenerated cells seemed to account for their inability to pass easily through the human trabecular meshwork and, therefore, to cause severe glaucoma.

Aged↗
PubMed2001

How does nonpenetrating glaucoma surgery work? Aqueous outflow resistance and glaucoma surgery.

Histologic, experimental, and theoretical studies of the aqueous outflow pathways point toward the juxtacanalicular region and inner wall of Schlemm's canal as the likely site of aqueous outflow resistance in the normal eye. At least 50% of the aqueous outflow resistance in the normal eye and the bulk of the pathologically increased resistance in the glaucomatous eye resides in the trabecular meshwork and the inner wall of Schlemm's canal. The uveoscleral, or uveovortex, pathway, which accounts for perhaps 10% of the aqueous drainage in the healthy aged human eye, can become a major accessory route for aqueous drainage after pharmacologic treatment. Surgeries designed to incise or remove the abnormal trabecular meshwork of glaucoma address the pathologic problem of the disease. Surgeries that unroof Schlemm's canal or expand the canal, such as viscocanalostomy, probably cause inadvertent ruptures of the inner wall and juxtacanalicular tissue, thus relieving the abnormal outflow resistance of glaucoma. This review is a summary of current thought on the pathophysiology of aqueous outflow resistance in glaucoma and, in light of this, provides an interpretation of the mechanism of pressure reduction created by these new surgeries.

Anterior Eye Segment↗
PubMed1984

Laser-induced primate glaucoma. II. Histopathology.

A sustained, moderate pressure elevation was produced in 15 nonhuman primate eyes by application of laser energy to the trabecular meshwork. By light and electron microscopy, the trabecular beams were blunted, and scattered synechiae were present. Backward bowing of the lamina cribrosa, partial loss of the myelin sheath surrounding axonal segments just posterior to the lamina, and diffuse axonal loss involving the entire nerve cross section were noted. A quantitative analysis of this axonal loss revealed that eyes with moderate nerve head damage (cup-disc ratio, 0.6 to 0.8) had only 38% to 69% of the expected normal axonal count. The eyes with nearly total cupping (cup-disc ratio, 0.9 to 1.0) maintained between 10% and 36% of the normal axonal count. The disc changes in these experimental eyes are similar to those previously described in human eyes with glaucoma.

Animals↗
PubMed2003

In vitro effects of preserved and unpreserved antiglaucoma drugs on apoptotic marker expression by human trabecular cells.

BACKGROUND: The mechanisms of trabecular cell loss in glaucoma patients are poorly understood. In order to determine whether drug-induced apoptosis could be one of the mechanisms by which trabecular cells die in glaucoma, we evaluated the effect of benzalkonium-preserved (BAC+) or preservative-free (BAC-) antiglaucoma medications on apoptotic marker expression by cultured human trabecular meshwork (HTM) cells. METHODS: Normal and glaucomatous trabecular cell lines were treated for 15 min with antiglaucoma drugs (1/100 and 1/10 dilutions): timolol BAC+ or BAC-, betaxolol BAC+ or BAC-, latanoprost BAC+ or pure BAC. Apo2.7 expression, annexin V binding and DNA content were evaluated by flow cytometry and confocal microscopy. RESULTS: Results obtained in the two cell lines were similar for all tested drugs and criteria. In a 1/100 dilution, unpreserved beta-blockers had no apoptotic effect, preserved beta-blockers and latanoprost significantly increased Apo2.7 expression only, while BAC significantly increased all three apoptotic markers. When tested in a 1/10 dilution, all drugs except unpreserved timolol triggered a 2- to 3.5-fold increase in apoptotic features, whereas up to 95% of the cells underwent apoptosis upon treatment with BAC (representing a 9-fold increase over the background level). CONCLUSION: At concentrations higher than those supposed to be found in the aqueous humor after instillation (1/100 dilution), unpreserved beta-blocker exhibited no proapoptotic activity on HTM cells in vitro. Benzalkonium-containing beta-blockers and prostaglandin analogue triggered mild expression of one out of three apoptotic markers, while the pro-apoptotic effect observed with BAC appeared to be largely hindered by active compounds in the preserved eyedrops.

Adolescent↗