Elevated Intraocular Pressure (elevated + intraocular_pressure)

Distribution by Scientific Domains


Selected Abstracts


Dexamethasone alters F-actin architecture and promotes cross-linked actin network formation in human trabecular meshwork tissue

CYTOSKELETON, Issue 2 2005
Abbot F. Clark
Abstract Elevated intraocular pressure is an important risk factor for the development of glaucoma, a leading cause of irreversible blindness. This ocular hypertension is due to increased hydrodynamic resistance to the drainage of aqueous humor through specialized outflow tissues, including the trabecular meshwork (TM) and the endothelial lining of Schlemm's canal. We know that glucocorticoid therapy can cause increased outflow resistance and glaucoma in susceptible individuals, that the cytoskeleton helps regulate aqueous outflow resistance, and that glucocorticoid treatment alters the actin cytoskeleton of cultured TM cells. Our purpose was to characterize the actin cytoskeleton of cells in outflow pathway tissues in situ, to characterize changes in the cytoskeleton due to dexamethasone treatment in situ, and to compare these with changes observed in cell culture. Human ocular anterior segments were perfused with or without 10,7 M dexamethasone, and F-actin architecture was investigated by confocal laser scanning microscopy. We found that outflow pathway cells contained stress fibers, peripheral actin staining, and occasional actin "tangles." Dexamethasone treatment caused elevated IOP in several eyes and increased overall actin staining, with more actin tangles and the formation of cross-linked actin networks (CLANs). The actin architecture in TM tissues was remarkably similar to that seen in cultured TM cells. Although CLANs have been reported previously in cultured cells, this is the first report of CLANs in tissue. These cytoskeletal changes may be associated with increased aqueous humor outflow resistance after ocular glucocorticoid treatment. Cell Motil. Cytoskeleton 60:83,95, 2005. © 2004 Wiley-Liss, Inc. [source]


Prostanoids in the Therapy of Glaucoma

CARDIOVASCULAR THERAPEUTICS, Issue 1 2006
Naruhiro Ishida
ABSTRACT Elevated intraocular pressure (IOP) is one of the most important risk factors for the development of glaucoma, which is a progressive optic neuropathy. Lowering IOP is currently the only therapeutic approach to the therapy of glaucoma. Since the use of pilocarpine eye drops for glaucoma treatment was reported in the late 1870s, academic researchers and pharmaceutical companies attempted to discover new drugs with more potent, prolonged, and safer IOP-reducing effects. These persistent efforts finally paid off, and prostanoids with FP-receptor agonist activity were found to be very potent IOP-lowering agents. To date, three prostanoids (latanoprost, travoprost and bimatoprost) have been launched in many countries, and now a new FP-receptor agonist, tafluprost, is entering clinical development. All of these prostanoids are superior to the ,-adrenoceptor antagonists in their IOP-lowering efficacy, and no severe side effects have been reported in their long-term clinical use. In addition, tafluprost may be expected to improve ocular blood flow. Hence, prostanoids currently occupy center stage among glaucoma medications. It cannot be denied that in terms of efficacy, safety, patient compliance, and medical economy prostanoids are currently the first-line medicines among ocular antihypertensive drugs. [source]


In vitro evaluation of reactive astrocyte migration, a component of tissue remodeling in glaucomatous optic nerve head

GLIA, Issue 3 2001
Gülgün Tezel
Abstract In order to improve understanding of remodeling events in the glaucomatous optic nerve head, the migration of optic nerve head astrocytes was studied in vitro. Since elevated intraocular pressure is an important stress factor identified in glaucomatous eyes, optic nerve head astrocytes were incubated under physical stress created by elevated hydrostatic pressure. In addition, they were incubated in the presence of a chemical stimulus, lipolysaccharide (LPS). Migration of reactivated astrocytes in the presence of these stressors was examined using chambers in which cell migration through extracellular matrix-coated pores is only possible following proteolytic digestion of the matrix. We observed that the migratory ability of optic nerve head astrocytes was approximately 4,6 times greater following exposure to elevated hydrostatic pressure or LPS for up to 48 h. Phosphoinositide 3-kinase, protein kinase C, and tyrosine kinase were found to be involved in the signal transduction for activated migration of optic nerve head astrocytes in response to elevated hydrostatic pressure or LPS. In addition, we observed that the stress-induced migration of optic nerve head astrocytes, which is accompanied by proteolytic degradation, resulted in the formation of culture cavities containing mucopolysaccharides. These in vitro findings provide a clearer understanding of the pathophysiologic mechanisms of characteristic tissue remodeling events that occur, in vivo, in the glaucomatous optic nerve head. GLIA 34:178,189, 2001. © 2001 Wiley-Liss, Inc. [source]


Subunits of the epithelial sodium channel family are differentially expressed in the retina of mice with ocular hypertension

JOURNAL OF NEUROCHEMISTRY, Issue 1 2005
Frank M. Dyka
Abstract Glaucoma is a prevalent cause of blindness, resulting in the apoptotic death of retinal ganglion cells and optic nerve degeneration. The disease is often associated with elevated intraocular pressure, however, molecular mechanisms involved in ganglion cell death are poorly understood. To identify proteins contributing to this pathological process, we analysed the retinal gene expression of DBA/2J mice that develop an elevated intraocular pressure by the age of 6 months with subsequent ganglion cell loss. In this study, we identified subunits of the epithelial sodium channel (ENaC) family that are specifically expressed under elevated intraocular pressure. Using reverse transcriptase polymerase chain reaction we observed a significant increase of ,-ENaC in the neuronal retina of DBA/2J mice when compared with control animals, while ,-ENaC and ,-ENaC were not detectable in this tissue. Specific immune sera to ENaC subunits showed up-regulation of ,-ENaC in synaptic and nuclear layers of the retina, and in the retinal pigment epithelium. Consistent with our polymerase chain reaction data, ,-ENaC was not detected by specific antibodies in the retina, while ,-ENaC was only present in the retinal pigment epithelium under ocular hypertension. Finally, the increase of ,-ENaC gene expression in the neuronal retina and the retinal pigment epithelium was not observed in other tissues of DBA/2J mice. Since the intraocular pressure is regulated by the transport of aqueous humour across epithelial structures of the eye that in turn is associated with ion flux, the specific up-regulation of ENaC proteins could serve as a protecting mechanism against elevated intraocular pressure. [source]


Primary glaucoma in Burmese cats

AUSTRALIAN VETERINARY JOURNAL, Issue 11 2002
ECGM HAMPSON
Objective To document the clinical signs and management of primary glaucoma in Burmese cats. Design A retrospective study of six affected Burmese cats, from 1996 to 2001. ProcedureSix Burmese cats diagnosed with primary glaucoma were managed over periods varying from 3 months to 4.5 years. Clinical details were obtained from practice records. Gonioscopic examination of the drainage or iridocorneal angle in eyes of these affected cats was made. ResultsSix desexed female Burmese cats (ages 7.0 to 10.5 years) presented with complaints of either unilateral (n = 4) or bilateral (n = 2) red eye, dilated pupil or enlarged eye. In one of the affected cats, one eye had been enucleated prior to the commencement of the study, thus a total of 11 eyes were examined. Clinically, all affected eyes (n = 8) had injected episcleral blood vessels and elevated intraocular pressure. Gonioscopy revealed the presence of nine narrow and two closed irido-corneal angles. Medical therapy included topical 2% dorzolamide (n = 8), 0.5% timolol maleate (n = 1), 0.005% latanoprost (n = 1) and 0.5,1.0% prednisolone acetate (n = 8). Surgery was performed in six eyes using either diode laser (n = 5) and/or cryothermy (n = 2) and one eye was eviscerated, with implantation of a prosthesis. With therapy, five affected eyes maintained vision and normal intraocular pressure, one eye remained blind with normal intraocular pressure, one eye remained blind with elevated intraocular pressure and one eye was eviscerated. Conclusions The Burmese cat may be predisposed to primary narrow-angle glaucoma. Early diagnosis and continuous antiglaucoma therapy can help control intraocular pressure and maintain vision. [source]


1262: Symptoms and signs of anterior uveitis

ACTA OPHTHALMOLOGICA, Issue 2010
I TUGAL-TUTKUN
Purpose Based on the anatomic classification of uveitis, iritis and iridocyclitis are classified as anterior uveitis. Methods Symptoms and signs of anterior uveitis will be presented Results Patients with acute anterior uveitis typically present with red eyes, photophobia, ocular pain, and sometimes visual blurring. In chronic anterior uveitis, onset is usually insidious and patients may be asymptomatic until the development of complications. Ciliary injection, endothelial dusting or fine keratic precipitates (KPs), cells and flare in the anterior chamber with or without hypopyon formation or fibrinous exudate are the typical findings of alternating unilateral acute nongranulomatous anterior uveitis which is most commonly seen in association with HLA-B27 antigen and spondyloarthropaties. Medium-size KPs or large mutton-fat KPs, chronic flare, Koeppe and Busacca nodules of the iris, peripheral anterior synechiae and broad-based posterior synechiae are the typical findings of granulomatous anterior uveitis which is often chronic. Viral anterior uveitis is characterized by unilateral recurrent episodes of anterior uveitis characterized by endotheliitis, elevated intraocular pressure, and patchy or sectoral iris atrophy. JIA-associated anterior uveitis is typically a bilateral nongranulomatous chronic anterior uveitis often complicated by band keratopathy, seclusion of the pupil, and cataract. Conclusion Symptoms and signs in anterior uveitis vary depending on the acute or chronic, ganulomatous or nongranulomatous nature of the disease. Specific anterior uveitic entities are characterized by a distinct constellation of ocular signs. [source]


Longterm results after phacovitrectomy and foldable intraocular lens implantation

ACTA OPHTHALMOLOGICA, Issue 8 2009
Wensheng Li
Abstract. Purpose:, This study aimed to evaluate the longterm results of phacovitrectomy and foldable intraocular lens (IOL) implantation in eyes with significant cataract and co-existing vitreoretinal diseases. Methods:, We carried out a retrospective study of 186 eyes of 149 patients with various vitreoretinal abnormalities and visually significant cataracts. Vitreoretinal surgery was combined with phacoemulsification and foldable IOL implantation. Main outcome measures were visual acuity (VA), preoperative data, and intraoperative and postoperative complications. Results:, The most common indications for surgery were non-diabetic vitreous haemorrhage and proliferative diabetic retinopathy. Preoperative vision ranged from 0.6 to light perception; postoperative vision ranged from 1.2 to no light perception. Postoperatively, in 162 eyes (87.1%) VA improved by , 3 lines on the decimal chart. In 14 eyes (7.5%), vision remained within 3 lines of preoperative levels and in 10 eyes (5.3%), vision had decreased by the last follow-up. Postoperative complications included elevated intraocular pressure and posterior capsule opacification, corneal edema, macular edema, fibrinous reaction, vitreous hemorrhage, corneal epithelial defects, anterior chamber hyphema, choroidal detachment, persistent macular hole, posterior synechiae, recurrent retinal detachment, rubeosis iridis, neovascular glaucoma. Conclusions:, Combined vitreoretinal surgery and phacoemulsification with foldable IOL implantation is safe and effective in treating vitreoretinal abnormalities co-existing with cataract. Based on extensive experience with the combined procedure, we suggest that combined surgery is recommended in selected patients with simultaneous vitreoretinal pathological changes and cataract. [source]


Disease mechanisms leading to impaired blood flow in glaucoma

ACTA OPHTHALMOLOGICA, Issue 2009
D GHERGHEL
Purpose SIS lecture Methods Literature search Results Although primary open-angle glaucoma (POAG), is associated more closely with elevated intraocular pressure (IOP), other risk factors already implicated in the aetiology of this disease and especially in the aetiology of normal-tension glaucoma are: abnormal ocular circulation, ocular and systemic vascular dysregulation, as well as systemic blood pressure (BP) alterations. Oxidative stress, which occurs as a result of an imbalance between generation of reactive oxygen species (ROS) and antioxidant defence mechanisms and is implicated in the pathogenesis of disorders ranging from atherosclerosis to neurodegenerative disorders, diabetes and aging, may also contribute to the general vascular disturbances observed in glaucoma. Moreover, increasing evidence shoes that oxidative stress plays a role in promoting endothelial dysfunction, which is a key factor in progression of vascular diseases. Indeed, glaucomatous optic nerve damage has been related to endothelial damage/dysfunction. This presentation explores the role of various ocular and systemic circulatory factors in the pathogenesis of glaucomatous neuropathy. [source]


Bevacizumab (Avastin) for the treatment of neovascular glaucoma

CLINICAL & EXPERIMENTAL OPHTHALMOLOGY, Issue 5 2007
Michael N Chilov MBBS
Abstract Herein three cases of angle closure secondary to neovascularization (elevated intraocular pressure in two of the cases) treated with the anti-vascular endothelial growth factor (VEGF) monoclonal antibody bevacizumab (Avastin) are reported. In all three cases there was rapid resolution of neovascularization and control of intraocular pressure. One patient with corneal anaesthesia from diabetes developed infectious keratitis, potentially as a consequence of inhibition of VEGF wound healing and neurotrophic functions. Avastin appears to have a promising role in the treatment of neovascular glaucoma but is not without potential local and systemic side-effects. [source]


Bilateral angle closure glaucoma induced by sulphonamide-derived medications

CLINICAL & EXPERIMENTAL OPHTHALMOLOGY, Issue 1 2007
Grace C Lee MD
Abstract Background:, Sulphonamide-derived medications are widely used, although not always recognized as such. We report the occurrence of bilateral angle closure glaucoma with sulphonamide-derived medications and highlight features of the presentation and treatment to assist in early diagnosis and management. Methods:, The clinical records of three cases with bilateral angle closure glaucoma induced by three sulphonamide-derived medications, sulfasalazine, oral acetazolamide, and hydrochlorothiazide, were reviewed. Results:, All three cases identified presented with bilateral angle closure glaucoma and persistent elevated intraocular pressure despite patent iridotomy. Patients may be pseudophakic (2) or phakic (1).Cessation of the suspected medication is necessary to reverse the mechanism. Conclusions:, The proposed mechanism of angle closure glaucoma induced by sulphonamide medication involves an idiosyncratic reaction in the uveal tissues to these systemic drugs that is associated with expansion of the extracellular tissue of the ciliary body and choroid. Management identification of sulphonamide-derived medications and immediate cessation of suspected sulphonamide-derived medication, refraction and ultrasound B scan or ultrasound biomicroscopy may aid in the proper diagnosis and can also be helpful for confirmation. [source]


Optic nerve blood flow in glaucoma

CLINICAL AND EXPERIMENTAL OPTOMETRY, Issue 3 2000
Renuka Bathija FRACO FRACS
Background: Glaucomatous optic neuropathy often occurs in the absence of elevated intraocular pressure and, conversely, elevated intraocular pressure may occur without associated damage of the optic nerve. These findings challenge the simple explanation of intraocular pressure being the sole cause of neural loss and have led to theories of ischaemic causes of the morbidity. This paper reviews the vascular anatomy of the optic disc, the factors that control its blood flow and the existing techniques for measurement of the blood flow. It also briefly discusses the possible role of apoptosis in glaucomatous visual loss. Method: Literature review. Conclusions: The posterior ciliary artery circulation is the main source of the blood supply to the optic nerve head with additional lesser supply via the central retinal artery and the choroidal circulation. There is considerable individual variation in the distribution of this circulation and complex regulatory systems govern its function. It is likely that microcirculatory changes in the vascular supply of the optic disc play a role in glaucoma, either as the primary abnormality or as a co-factor that increases susceptibility to damage from increased intraocular pressure through impaired auto-regulation. Clinical trials are currently in progress for the treatment of glaucoma with systemically administered agents that are antagonists of the receptors that mediate glutamine toxicity, a factor in the process of apoptosis. [source]