scholarly journals Acute Effects of Intraocular Pressure-Induced Changes in Schlemm's Canal Morphology on Outflow Facility in Healthy Human Eyes

2020 ◽  
Vol 61 (8) ◽  
pp. 36
Author(s):  
Wei Chen ◽  
Tian Hu ◽  
Qiongfang Xu ◽  
Zhiqi Chen ◽  
Hong Zhang ◽  
...  
Keyword(s):  
Intraocular Pressure ◽  
Acute Effects ◽  
Schlemm’S Canal ◽  
Healthy Human ◽  
Outflow Facility ◽  
Schlemm's Canal ◽  
Induced Changes ◽  
Human Eyes ◽  
Canal Morphology

scholarly journals Sphingosine-1-phosphate effects on the inner wall of Schlemm's canal and outflow facility in perfused human eyes

2009 ◽  
Vol 89 (6) ◽  
pp. 980-988 ◽  
Author(s):  
W. Daniel Stamer ◽  
A. Thomas Read ◽  
Grant M. Sumida ◽  
C. Ross Ethier
Keyword(s):  
Schlemm’S Canal ◽  
Outflow Facility ◽  
Schlemm's Canal ◽  
Sphingosine 1 Phosphate ◽  
Human Eyes

Pharmacologic Disruption of Schlemm’s Canal Cells and Outflow Facility in Anterior Segments of Human Eyes

2004 ◽  
Vol 45 (7) ◽  
pp. 2246 ◽  
Author(s):  
Cindy K. Bahler ◽  
Cheryl R. Hann ◽  
Michael P. Fautsch ◽  
Douglas H. Johnson
Keyword(s):  
Schlemm’S Canal ◽  
Outflow Facility ◽  
Schlemm's Canal ◽  
Anterior Segments ◽  
Human Eyes

scholarly journals Morphological changes in the trabecular meshwork and Schlemm’s canal after treatment with topical intraocular pressure-lowering agents

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ji-Hye Park ◽  
Hyun Woo Chung ◽  
Eun Gyu Yoon ◽  
Min Jung Ji ◽  
Chungkwon Yoo ◽  
...  
Keyword(s):  
Intraocular Pressure ◽  
Trabecular Meshwork ◽  
Morphological Changes ◽  
Open Angle Glaucoma ◽  
Anterior Segment ◽  
Schlemm’S Canal ◽  
Schlemm's Canal ◽  
Before And After ◽  
Treatment Naïve ◽  
Aqueous Outflow

AbstractGlaucoma treatment is usually initiated with topical medication that lowers the intraocular pressure (IOP) by reducing the aqueous production, enhancing the aqueous outflow, or both. However, the effect of topical IOP-lowering medications on the microstructures of the aqueous outflow pathway are relatively unknown. In this retrospective, observational study, 56 treatment-naïve patients with primary open-angle glaucoma were enrolled. Images of the nasal and temporal corneoscleral limbus were obtained using anterior segment optical coherence tomography (AS-OCT). The conjunctival vessels and iris anatomy were used as landmarks to select the same limbal area scan, and the trabecular meshwork (TM) width, TM thickness, and Schlemm’s canal (SC) area were measured before and after using the IOP-lowering agents for 3 months. Among the 56 patients enrolled, 33 patients used prostaglandin (PG) analogues, and 23 patients used dorzolamide/timolol fixed combination (DTFC). After 3 months of DTFC usage, the TM width, TM thickness, and SC area did not show significant changes in either the nasal or temporal sectors. Conversely, after prostaglandin analog usage, the TM thickness significantly increased, and the SC area significantly decreased (all P < 0.01). These findings warrant a deeper investigation into their relationship to aqueous outflow through the conventional and unconventional outflow pathways after treatment with PG analogues.

scholarly journals Simultaneous influence of sympathetic autonomic stress on Schlemm’s canal, intraocular pressure and ocular circulation

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Wei Chen ◽  
Zhiqi Chen ◽  
Yan Xiang ◽  
Chaohua Deng ◽  
Hong Zhang ◽  
...  
Keyword(s):  
Intraocular Pressure ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Retinal Vessel ◽  
Cross Sectional Area ◽  
Sectional Area ◽  
Schlemm’S Canal ◽  
Cold Stimulation ◽  
Cross Sectional ◽  
Schlemm's Canal

AbstractThis study aimed to investigate changes in Schlemm’s canal, intraocular pressure and ocular blood circulation following the activation of the sympathetic nervous system. Twenty healthy volunteers were enrolled in this study. The cold pressor test (CPT) was adopted. Cross-sectional area of Schlemm’s canal (SCAR), superficial and deep retinal vessel densities (s-RVD;d-RVD), pupil diameter (PD), intraocular pressure (IOP), mean ocular perfusion pressure (MOPP) and heart rate variability (HRV) were measured at three time-points: baseline (T0) and 5 min (T1) and 10 min (T2) after the CPT. After cold stimulation, LF/HF index (the ratio of low frenquency and high frenquency) increased significantly. IOP decreased from 16.9 ± 1.9 mmHg at baseline to 16.4 ± 2.7 mmHg at T1 and to 15.2 ± 2.7 mmHg at T2. The nasal cross-sectional area of SCAR (SCAR-n) increased from 6283.9 ± 2696.2 µm2 at baseline to 8392.9 ± 3258.7 µm2 at T1 and to 10422.0 ± 3643.8 µm2 at T2. The temporal cross-sectional area of SCAR (SCAR-t) increased from 6414.5 ± 2218.7 µm2 at baseline to 8610.8 ± 2317.1 µm2 at T1 and to 11544.0 ± 4129.2 µm2 at T2. The expansion of Schlemm’s canal was observed after the CPT might be caused by sympathetic nerve stimulation, subsequently leading to decreased IOP.

scholarly journals Shear Stress in Schlemm’s Canal as a Sensor of Intraocular Pressure

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Fiona McDonnell ◽  
Kristin M. Perkumas ◽  
Nicole E. Ashpole ◽  
Joan Kalnitsky ◽  
Joseph M. Sherwood ◽  
...  
Keyword(s):  
Shear Stress ◽  
Intraocular Pressure ◽  
Schlemm’S Canal ◽  
Schlemm's Canal

scholarly journals Role of nitric oxide in murine conventional outflow physiology

2015 ◽  
Vol 309 (4) ◽  
pp. C205-C214 ◽  
Author(s):  
Jason Y. H. Chang ◽  
W. Daniel Stamer ◽  
Jacques Bertrand ◽  
A. Thomas Read ◽  
Catherine M. Marando ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Fluorescent Protein ◽  
Detectable Effect ◽  
No Production ◽  
Schlemm’S Canal ◽  
Physiological Regulation ◽  
Outflow Facility ◽  
Aqueous Humor Outflow ◽  
Schlemm's Canal

Elevated intraocular pressure (IOP) is the main risk factor for glaucoma. Exogenous nitric oxide (NO) decreases IOP by increasing outflow facility, but whether endogenous NO production contributes to the physiological regulation of outflow facility is unclear. Outflow facility was measured by pressure-controlled perfusion in ex vivo eyes from C57BL/6 wild-type (WT) or transgenic mice expressing human endothelial NO synthase (eNOS) fused to green fluorescent protein (GFP) superimposed on the endogenously expressed murine eNOS (eNOS-GFPtg). In WT mice, exogenous NO delivered by 100 μM S-nitroso- N-acetylpenicillamine (SNAP) increased outflow facility by 62 ± 28% (SD) relative to control eyes perfused with the inactive SNAP analog N-acetyl-d-penicillamine (NAP; n = 5, P = 0.016). In contrast, in eyes from eNOS-GFPtg mice, SNAP had no effect on outflow facility relative to NAP (−9 ± 4%, P = 0.40). In WT mice, the nonselective NOS inhibitor NG-nitro-l-arginine methyl ester (l-NAME, 10 μM) decreased outflow facility by 36 ± 13% ( n = 5 each, P = 0.012), but 100 μM l-NAME had no detectable effect on outflow facility (−16 ± 5%, P = 0.22). An eNOS-selective inhibitor (cavtratin, 50 μM) decreased outflow facility by 19 ± 12% in WT ( P = 0.011) and 39 ± 25% in eNOS-GFPtg ( P = 0.014) mice. In the conventional outflow pathway of eNOS-GFPtg mice, eNOS-GFP expression was localized to endothelial cells lining Schlemm's canal and the downstream vessels, with no apparent expression in the trabecular meshwork. These results suggest that endogenous NO production by eNOS within endothelial cells of Schlemm's canal or downstream vessels contributes to the physiological regulation of aqueous humor outflow facility in mice, representing a viable strategy to more successfully lower IOP in glaucoma.

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