scholarly journals Role of prostaglandins and specific place in therapy of bimatoprost in the treatment of elevated intraocular pressure and ocular hypertension: A closer look at the agonist properties of bimatoprost and the prostamides

2009 ◽  
pp. 663 ◽  
Author(s):  
Scott Smid
Keyword(s):  
Intraocular Pressure ◽  
Ocular Hypertension ◽  
Elevated Intraocular Pressure

scholarly journals Experimental reproduction of the glaucomatous process

2013 ◽  
Vol 6 (3) ◽  
pp. 43-50 ◽  
Author(s):  
Ilmira Rifovna Gazizova ◽  
Vladimir Nikolayevich Alekseyev ◽  
Dmitriy Nikolayevich Nikitin
Keyword(s):  
Intraocular Pressure ◽  
Ocular Hypertension ◽  
Experimental Studies ◽  
Pressure Level ◽  
Trophic Factors ◽  
Experimental Reproduction ◽  
Experimental Animals ◽  
New Knowledge ◽  
The Brain

The glaucomatous process is one of the important challenges in ophthalmology. And this is due primarily to the fact that, so far, the main causes for the onset and progression of glaucoma are not been fully determined. Numerous experimental studies concentrate on the role of ocular hypertension. However, there are forms of glaucoma, which are independent of the intraocular pressure level. A better experimental model for the study of glaucoma would also take into consideration the development of the characteristic complex of signs, in which a key sign would be a slowly progressing optic disc excavation. Therefore, taking into account the new knowledge in the pathogenesis of neurodegenerative changes in glaucoma, the ability to investigate the brain, vascular factors of progression, the level of neurotransmitters, trophic factors, etc. should be added to this model. Therefore we tried to make an analysis of glaucoma models in various experimental animals to find most appropriate models to study the aspects of glaucoma pathogenesis.

Design of Experiments for Exposure of Astrocytes to Elevated Hydrostatic Pressure and Hypoxia

2008 ◽  
Author(s):  
Shadi Rajabi ◽  
Craig A. Simmons ◽  
C. Ross Ethier
Keyword(s):  
Intraocular Pressure ◽  
Visual Field ◽  
Retinal Ganglion Cells ◽  
Vision Loss ◽  
Ganglion Cells ◽  
Visual Field Loss ◽  
Retinal Ganglion ◽  
Common Cause ◽  
Elevated Intraocular Pressure

Glaucoma, a chronic optic neuropathy, is the second most common cause of blindness, affecting 67 million people worldwide. The damage in glaucoma occurs at the optic nerve head (ONH), where the axons of the retinal ganglion cells leave the eye posteriorly. Glaucoma is frequently associated with elevated intraocular pressure (IOP), and visual field loss can be prevented by significant lowering of IOP. Hence, the role of pressure in glaucoma is important. Unfortunately, the mechanism by which pressure leads to vision loss in glaucoma is very poorly understood.

scholarly journals What was Glaucoma Called before the 20th Century?

2015 ◽  
Vol 7 ◽  
pp. OED.S32004 ◽  
Author(s):  
Christopher T. Leffler ◽  
Stephen G. Schwartz ◽  
Francesca M. Giliberti ◽  
Matthew T. Young ◽  
Dennis Bermudez
Keyword(s):  
Intraocular Pressure ◽  
Optic Neuropathy ◽  
Primary Open Angle Glaucoma ◽  
Open Angle Glaucoma ◽  
The Other ◽  
Angle Closure ◽  
Open Angle ◽  
Poor Vision ◽  
Elevated Intraocular Pressure

Glaucoma involves a characteristic optic neuropathy, often with elevated intraocular pressure. Before 1850, poor vision with a normal eye appearance, as occurs in primary open-angle glaucoma, was termed amaurosis, gutta serena, or black cataract. Few observers noted palpable hardness of the eye in amaurosis. On the other hand, angle-closure glaucoma can produce a green or gray pupil, and therefore was called, variously, glaucoma (derived from the Greek for glaucous, a nonspecific term connoting blue, green, or light gray) and viriditate oculi. Angle closure, with palpable hardness of the eye, mydriasis, and anterior prominence of the lens, was described in greater detail in the 18th and 19th centuries. The introduction of the ophthalmoscope in 1850 permitted the visualization of the excavated optic neuropathy in eyes with a normal or with a dilated greenish-gray pupil. Physicians developed a better appreciation of the role of intraocular pressure in both conditions, which became subsumed under the rubric “glaucoma”.

Role of adenosine receptors in resveratrol-induced intraocular pressure lowering in rats with steroid-induced ocular hypertension

2014 ◽  
Vol 43 (1) ◽  
pp. 54-66 ◽  
Author(s):  
Norhafiza Razali ◽  
Renu Agarwal ◽  
Puneet Agarwal ◽  
Sunil Kumar ◽  
Minaketan Tripathy ◽  
...  
Keyword(s):  
Intraocular Pressure ◽  
Ocular Hypertension ◽  
Adenosine Receptors ◽  
Pressure Lowering

scholarly journals Novel free radical scavengers protect retinal cells and decrease elevated intraocular pressure in a rat ocular hypertension model

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Alireza Hosseini ◽  
Frank A. Lattanzio ◽  
Karl A. Schellenberg ◽  
Sandeep S Samudre ◽  
James Shaeffer ◽  
...  
Keyword(s):  
Intraocular Pressure ◽  
Free Radical ◽  
Ocular Hypertension ◽  
Free Radical Scavengers ◽  
Radical Scavengers ◽  
Retinal Cells ◽  
Elevated Intraocular Pressure

scholarly journals Clinical Options for the Reduction of Elevated Intraocular Pressure

2012 ◽  
Vol 4 ◽  
pp. OED.S4909 ◽  
Author(s):  
Laura Crawley ◽  
Sohaib M. Zamir ◽  
Maria F. Cordeiro ◽  
Li Guo
Keyword(s):  
Intraocular Pressure ◽  
Clinical Practice ◽  
Chronic Disease ◽  
Ocular Hypertension ◽  
New Technologies ◽  
Pharmacological Agents ◽  
Elevated Intraocular Pressure ◽  
Laser Treatments

Elevated IOP in clinical practice is usually seen in glaucoma or ocular hypertension. Glaucoma affects 60 million people worldwide and 8.4 million are bilaterally blind from this chronic disease. 1 Options for reducing IOP rely on pharmacological agents, laser treatments and surgery which may be penetrating or non-penetrating. The last twenty years has seen significant changes in all of these strategies. This review aims to cover these clinical options and introduce some of the new technologies currently in development for the clinical lowering of IOP.

scholarly journals Fibronectin extra domain A (FN-EDA) elevates intraocular pressure through Toll-like receptor 4 signaling

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Amanda L. Roberts ◽  
Timur A. Mavlyutov ◽  
Tanisha E. Perlmutter ◽  
Stacy M. Curry ◽  
Sherri L. Harris ◽  
...  
Keyword(s):  
Intraocular Pressure ◽  
Ocular Hypertension ◽  
Open Angle Glaucoma ◽  
Mouse Strains ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Aqueous Humor Outflow ◽  
Tlr4 Ligand ◽  
Constitutively Active

Abstract Elevated intraocular pressure (IOP) is a major risk factor for the development and progression of primary open angle glaucoma and is due to trabecular meshwork (TM) damage, which leads to impaired aqueous humor outflow. Here, we explore a novel molecular mechanism involved in glaucomatous TM damage. We investigated the role of an endogenous Toll-like receptor 4 (TLR4) ligand, fibronectin-EDA (FN-EDA), in TGFβ2-induced ocular hypertension in mice. We utilized transgenic mouse strains that either constitutively express only FN containing the EDA isoform or contain an EDA-null allele and express only FN lacking EDA, with or without a mutation in Tlr4, in our inducible mouse model of ocular hypertension by injection of Ad5.TGFβ2. IOP was measured over time and eyes accessed by immunohistochemistry for total FN and FN-EDA expression. Constitutively active EDA caused elevated IOP starting at 14 weeks of age. Ad5.TGFβ2 induced ocular hypertension in wildtype C57BL/6J mice and further amplified the IOP in constitutively active EDA mice. TLR4 null and EDA null mice blocked Ad5.TGFβ-induced ocular hypertension. Total FN and FN-EDA isoform expression increased in response to Ad5.TGFβ2. These data suggest that both TLR4 and FN-EDA contribute to TGFβ2 induced ocular hypertension.

Endothelial Tyrosine Kinase Tie1 Is Required for Normal Schlemm’s Canal Development

2022 ◽  
Author(s):  
Jing Du ◽  
Benjamin R. Thomson ◽  
Tuncer Onay ◽  
Susan E. Quaggin
Keyword(s):  
Intraocular Pressure ◽  
Quantitative Polymerase Chain Reaction ◽  
Schlemm’S Canal ◽  
Knock Out ◽  
Schlemm's Canal ◽  
Elevated Intraocular Pressure ◽  
Knock Out Mice ◽  
And Function ◽  
The Impact

Background: Schlemm’s canal (SC) is a large vessel residing in the iridocorneal angle and is required to regulate aqueous humor outflow. Normal SC structure and function is indispensable for maintaining normal intraocular pressure, and elevated intraocular pressure is a risk factor for development of glaucoma. Recent reports have identified a key role of the angiopoietin-Tie2 pathway for SC development and function; however, the role of the orphan receptor Tie1 has not been clarified. Methods: We used Tie1 knock out mice to study the function of Tie1 in SC development and function. Real-time quantitative polymerase chain reaction and Western blot analyses were used to verify Tie1 deletion. High-resolution microscopy of mouse SC whole mount and cross sections were used to study SC morphology. Measurement of intraocular pressure in live mice was used to study the impact of Tie1 on SC function. Results: Tie1 is highly expressed in both human and mouse SC. Tie1 knock out mice display hypomorphic SC and elevated intraocular pressure as a result of attenuated SC development. Conclusions: Tie1 is indispensable for SC development and function, supporting it as a novel target for future SC-targeted glaucoma therapies and a candidate gene for glaucoma in humans.

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