Aqueous outflow regulation: Optical coherence tomography implicates pressure-dependent tissue motion

Chen Xin, Ruikang K. Wang, Shaozhen Song, Tueng Shen, Joanne Wen, Elizabeth Martin, Yi Jiang, Steven Padilla, Murray Johnstone

Research output: Contribution to journalReview article

11 Citations (Scopus)

Abstract

Glaucoma is a leading cause of blindness worldwide and results from damage to the optic nerve. Currently, intraocular pressure is the only treatable risk factor. Changes in aqueous outflow regulate pressure; regulation becomes abnormal in glaucoma. From inside the eye aqueous flows out through the trabecular meshwork into a venous sinus called Schlemm's canal, next into collector channels and finally returns to the episcleral vessels of the venous system. The location of aqueous outflow regulation is unknown. Ex vivo and in vivo studies implicate both pressure-dependent trabecular tissue motion and tissues distal to Schlemm's canal in regulation of aqueous outflow. Technologies have not previously been available to study these issues. New ex vivo imaging in human eyes identifies hinged flaps or leaflets at collector channel entrances using a high-resolution spectral domain optical coherence tomography (SD-OCT) platform. The hinged flaps open and close in synchrony with pressure-dependent trabecular meshwork motion. The SD-OCT platform images from the trabecular meshwork surface while experimentally changing transtrabecular pressure gradients. New in vivo imaging in human eyes uses a motion sensitive technology, phase-sensitive OCT to quantitate real-time pulse-dependent trabecular tissue motion as well as absence of such motion when aqueous access to the outflow system is blocked. The recent studies suggest that aqueous outflow regulation results from synchronous pressure-dependent motion involving a network of interconnected tissues including those distal to Schlemm's canal. The new imaging technologies may shed light on glaucoma mechanisms and provide guidance in the management of medical, laser and surgical decisions in glaucoma.

Original languageEnglish (US)
Pages (from-to)171-186
Number of pages16
JournalExperimental Eye Research
Volume158
DOIs
StatePublished - May 1 2017
Externally publishedYes

Fingerprint

Optical Coherence Tomography
Trabecular Meshwork
Pressure
Glaucoma
Technology
Blindness
Optic Nerve
Intraocular Pressure
Lasers

Keywords

  • Aqueous
  • Collector channels
  • Glaucoma
  • Intraocular pressure
  • Lymphatics
  • Optical coherence tomography
  • Pulsatile flow
  • Schlemm's canal
  • Trabecular meshwork

ASJC Scopus subject areas

  • Ophthalmology
  • Sensory Systems
  • Cellular and Molecular Neuroscience

Cite this

Aqueous outflow regulation : Optical coherence tomography implicates pressure-dependent tissue motion. / Xin, Chen; Wang, Ruikang K.; Song, Shaozhen; Shen, Tueng; Wen, Joanne; Martin, Elizabeth; Jiang, Yi; Padilla, Steven; Johnstone, Murray.

In: Experimental Eye Research, Vol. 158, 01.05.2017, p. 171-186.

Research output: Contribution to journalReview article

Xin, Chen ; Wang, Ruikang K. ; Song, Shaozhen ; Shen, Tueng ; Wen, Joanne ; Martin, Elizabeth ; Jiang, Yi ; Padilla, Steven ; Johnstone, Murray. / Aqueous outflow regulation : Optical coherence tomography implicates pressure-dependent tissue motion. In: Experimental Eye Research. 2017 ; Vol. 158. pp. 171-186.
@article{af60810d48c3451ab11650521dadc4b9,
title = "Aqueous outflow regulation: Optical coherence tomography implicates pressure-dependent tissue motion",
abstract = "Glaucoma is a leading cause of blindness worldwide and results from damage to the optic nerve. Currently, intraocular pressure is the only treatable risk factor. Changes in aqueous outflow regulate pressure; regulation becomes abnormal in glaucoma. From inside the eye aqueous flows out through the trabecular meshwork into a venous sinus called Schlemm's canal, next into collector channels and finally returns to the episcleral vessels of the venous system. The location of aqueous outflow regulation is unknown. Ex vivo and in vivo studies implicate both pressure-dependent trabecular tissue motion and tissues distal to Schlemm's canal in regulation of aqueous outflow. Technologies have not previously been available to study these issues. New ex vivo imaging in human eyes identifies hinged flaps or leaflets at collector channel entrances using a high-resolution spectral domain optical coherence tomography (SD-OCT) platform. The hinged flaps open and close in synchrony with pressure-dependent trabecular meshwork motion. The SD-OCT platform images from the trabecular meshwork surface while experimentally changing transtrabecular pressure gradients. New in vivo imaging in human eyes uses a motion sensitive technology, phase-sensitive OCT to quantitate real-time pulse-dependent trabecular tissue motion as well as absence of such motion when aqueous access to the outflow system is blocked. The recent studies suggest that aqueous outflow regulation results from synchronous pressure-dependent motion involving a network of interconnected tissues including those distal to Schlemm's canal. The new imaging technologies may shed light on glaucoma mechanisms and provide guidance in the management of medical, laser and surgical decisions in glaucoma.",
keywords = "Aqueous, Collector channels, Glaucoma, Intraocular pressure, Lymphatics, Optical coherence tomography, Pulsatile flow, Schlemm's canal, Trabecular meshwork",
author = "Chen Xin and Wang, {Ruikang K.} and Shaozhen Song and Tueng Shen and Joanne Wen and Elizabeth Martin and Yi Jiang and Steven Padilla and Murray Johnstone",
year = "2017",
month = "5",
day = "1",
doi = "10.1016/j.exer.2016.06.007",
language = "English (US)",
volume = "158",
pages = "171--186",
journal = "Experimental Eye Research",
issn = "0014-4835",
publisher = "Academic Press Inc.",

}

TY - JOUR

T1 - Aqueous outflow regulation

T2 - Optical coherence tomography implicates pressure-dependent tissue motion

AU - Xin, Chen

AU - Wang, Ruikang K.

AU - Song, Shaozhen

AU - Shen, Tueng

AU - Wen, Joanne

AU - Martin, Elizabeth

AU - Jiang, Yi

AU - Padilla, Steven

AU - Johnstone, Murray

PY - 2017/5/1

Y1 - 2017/5/1

N2 - Glaucoma is a leading cause of blindness worldwide and results from damage to the optic nerve. Currently, intraocular pressure is the only treatable risk factor. Changes in aqueous outflow regulate pressure; regulation becomes abnormal in glaucoma. From inside the eye aqueous flows out through the trabecular meshwork into a venous sinus called Schlemm's canal, next into collector channels and finally returns to the episcleral vessels of the venous system. The location of aqueous outflow regulation is unknown. Ex vivo and in vivo studies implicate both pressure-dependent trabecular tissue motion and tissues distal to Schlemm's canal in regulation of aqueous outflow. Technologies have not previously been available to study these issues. New ex vivo imaging in human eyes identifies hinged flaps or leaflets at collector channel entrances using a high-resolution spectral domain optical coherence tomography (SD-OCT) platform. The hinged flaps open and close in synchrony with pressure-dependent trabecular meshwork motion. The SD-OCT platform images from the trabecular meshwork surface while experimentally changing transtrabecular pressure gradients. New in vivo imaging in human eyes uses a motion sensitive technology, phase-sensitive OCT to quantitate real-time pulse-dependent trabecular tissue motion as well as absence of such motion when aqueous access to the outflow system is blocked. The recent studies suggest that aqueous outflow regulation results from synchronous pressure-dependent motion involving a network of interconnected tissues including those distal to Schlemm's canal. The new imaging technologies may shed light on glaucoma mechanisms and provide guidance in the management of medical, laser and surgical decisions in glaucoma.

AB - Glaucoma is a leading cause of blindness worldwide and results from damage to the optic nerve. Currently, intraocular pressure is the only treatable risk factor. Changes in aqueous outflow regulate pressure; regulation becomes abnormal in glaucoma. From inside the eye aqueous flows out through the trabecular meshwork into a venous sinus called Schlemm's canal, next into collector channels and finally returns to the episcleral vessels of the venous system. The location of aqueous outflow regulation is unknown. Ex vivo and in vivo studies implicate both pressure-dependent trabecular tissue motion and tissues distal to Schlemm's canal in regulation of aqueous outflow. Technologies have not previously been available to study these issues. New ex vivo imaging in human eyes identifies hinged flaps or leaflets at collector channel entrances using a high-resolution spectral domain optical coherence tomography (SD-OCT) platform. The hinged flaps open and close in synchrony with pressure-dependent trabecular meshwork motion. The SD-OCT platform images from the trabecular meshwork surface while experimentally changing transtrabecular pressure gradients. New in vivo imaging in human eyes uses a motion sensitive technology, phase-sensitive OCT to quantitate real-time pulse-dependent trabecular tissue motion as well as absence of such motion when aqueous access to the outflow system is blocked. The recent studies suggest that aqueous outflow regulation results from synchronous pressure-dependent motion involving a network of interconnected tissues including those distal to Schlemm's canal. The new imaging technologies may shed light on glaucoma mechanisms and provide guidance in the management of medical, laser and surgical decisions in glaucoma.

KW - Aqueous

KW - Collector channels

KW - Glaucoma

KW - Intraocular pressure

KW - Lymphatics

KW - Optical coherence tomography

KW - Pulsatile flow

KW - Schlemm's canal

KW - Trabecular meshwork

UR - http://www.scopus.com/inward/record.url?scp=84978524006&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84978524006&partnerID=8YFLogxK

U2 - 10.1016/j.exer.2016.06.007

DO - 10.1016/j.exer.2016.06.007

M3 - Review article

C2 - 27302601

AN - SCOPUS:84978524006

VL - 158

SP - 171

EP - 186

JO - Experimental Eye Research

JF - Experimental Eye Research

SN - 0014-4835

ER -