The filtration characteristics of the aqueous outflow system

Johnson, Mark; Johnson, Douglas H.; Kamm, Roger D.; DeKater, Annelies W.; Epstein, David L.

doi:10.1016/0014-4835(90)90142-h

Cited by 46 publications

(25 citation statements)

References 17 publications

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“…It was found in these studies that a filtration barrier existed for particles larger than roughly one half micrometer or so, and thus it was concluded that pores nearly one micrometer in size must exist. More recent studies have confirmed this conclusion using microparticles and latex microspheres (Huggert, 1955;Huggert et al, 1955;Karg et al, 1959;Johnson et al, 1990). …”

Section: The Inner Wall Endothelium Of Schlemm's Canalsupporting

confidence: 59%

“…Nor has any alternate explanation been offered for the relatively easy passage of microparticles 200-500 nm in diameter through the outflow pathway (Johnson et al, 1990), except through these large pores. Since there are intact tight junctions between the inner wall cells (presumably to prevent blood reflux into the eye that can occur during periods of transient increases in ocular venous pressure), there are no other structures apparent in this endothelium that could explain the high hydraulic conductivity of this tissue or its filtration characteristics.…”

Section: The Inner Wall Endothelium Of Schlemm's Canalmentioning

confidence: 99%

See 1 more Smart Citation

‘What controls aqueous humour outflow resistance?’

Johnson

2006

Experimental Eye Research

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The bulk of aqueous humour outflow resistance is generated in or near the inner wall endothelium of Schlemm's canal in normal eyes, and probably also in glaucomatous eyes. Fluid flow through this region is controlled by the location of the giant vacuoles and pores found in cells of the endothelium of Schlemm's canal, but the flow resistance itself is more likely generated either in the extracellular matrix of the juxtacanalicular connective tissue or the basement membrane of Schlemm's canal. Future studies utilizing in vitro perfusion studies of inner wall endothelial cells may give insights into the process by which vacuoles and pores form in this unique endothelium and why inner wall pore density is greatly reduced in glaucoma. Keywordsglaucoma; Schlemm's canal; hydraulic conductivity It has been recognized for more that 130 years that the elevated pressure characteristic of primary open-angle glaucoma arises due to an increased resistance to the outflow of aqueous humour from the eye. (Leber, 1873) However, a conclusive determination of where in the outflow pathways this elevated outflow resistance is generated has been elusive. Surprisingly, the locus of aqueous humour outflow resistance in the normal eye has also been not been unequivocally determined.Seidel (1921) using light microscopy, stated 'that the inner wall of Schlemm's canal stand in open communication with the anterior chamber, and that the aqueous humour directly washes around the inner wall endothelium of Schlemm's canal and is only separated from the lumen of Schlemm's canal by a thin, outer membrane'. Our view is little different today. The locus of outflow resistance, both in the normal eye and the glaucomatous eye, is thought to arise either in the endothelial lining of Schlemm's canal, or very near to this location. In this article, current thoughts on where that flow resistance might be generated are reviewed.There are a number of excellent review articles (Tripathi, 1974a,b;Bill, 1975;Bill and Mäepea, 1994;Gong et al., 1996;Johnson and Erickson, 2000;Ethier, 2002) that describe the detailed morphology and physiology of the aqueous outflow pathway. In this review, the evidence that leads to the conclusion that the inner wall region is responsible for the bulk of aqueous humour outflow resistance is first presented. Then, attention is focused on those proximal aspects of this pathway that are nearest to the endothelial linings of Schlemm's canal, and the transport characteristics of these structures.The bulk of the aqueous humour flows out of the anterior chamber of the eye through the conventional aqueous outflow pathway comprised of the trabecular meshwork, the juxtacanalicular connective tissue, the endothelial lining of Schlemm's canal, Schlemm's canal itself, the collecting channels and aqueous veins, and then finally drains into the episcleral NIH Public Access NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript venous system, rejoining the blood from whence it came (in this review, the juxtacanalicular...

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Section: The Inner Wall Endothelium Of Schlemm's Canalsupporting

confidence: 59%

Section: The Inner Wall Endothelium Of Schlemm's Canalmentioning

confidence: 99%

‘What controls aqueous humour outflow resistance?’

Johnson

2006

Experimental Eye Research

Self Cite

403

366

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“…Studies utilizing tracer particles including zymosan, latex microspheres, cationic ferritin, and fluorescent Qdots indicated that segmental variations in outflow exist. (Battista et al, 2008; Buller et al, 1990; de Kater et al, 1989; Ethier and Chan, 2001; Hann et al, 2005; Hann and Fautsch, 2009; Johnson et al, 1990; Keller et al, 2011; Lu et al, 2008; Lu et al, 2011) The TM can therefore be separated into regions of high and low outflow, which appears to be consistent across species (human, monkeys, bovine, mice). Logically, there must be molecular differences between the components of each region that either affect or reflect the geographical outflow pathways.…”

Section: Function Of the Tmmentioning

confidence: 94%

Extracellular matrix in the trabecular meshwork: Intraocular pressure regulation and dysregulation in glaucoma

Vranka

Kelley

Acott

et al. 2015

Experimental Eye Research

299

291

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The trabecular meshwork (TM) is located in the anterior segment of the eye and is responsible for regulating the outflow of aqueous humor. Increased resistance to aqueous outflow causes intraocular pressure to increase, which is the primary risk factor for glaucoma. TM cells reside on a series of fenestrated beams and sheets through which the aqueous humor flows to exit the anterior chamber via Schlemm’s canal. The outer trabecular cells are phagocytic and are thought to function as a pre-filter. However, most of the outflow resistance is thought to be from the extracellular matrix (ECM) of the juxtacanalicular region, the deepest portion of the TM, and from the inner wall basement membrane of Schlemm’s canal. It is becoming increasingly evident that the extracellular milieu is important in maintaining the integrity of the TM. Not only have ultrastructural changes been observed in the ECM of the TM in glaucoma, and a significant number of mutations in ECM genes are known to be associated with glaucoma, but the stiffness of glaucomatous TM appears to be greater than that of normal tissue. Additionally, TGFβ2 has been found to be elevated in the aqueous humor of glaucoma patients and is assumed to be involved in ECM changes deep with the juxtacanalicular region of the TM. This review summarizes the current literature on trabecular ECM as well as the development and function of the TM. Animal models and organ culture models targeting specific ECM molecules to investigate the mechanisms of glaucoma are described. Finally, the growing number of mutations that have been identified in ECM genes and genes that modulate ECM in humans with glaucoma are documented.

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“…[36][37][38] More recently, microspheres of 0.18 m and 1.1 m diameter, perfused at concentrations of 3-5 × 10 5 and 3 × 10 3 per ml, were thought to be captured in the filtration system because of sticking to the tissue and not as a function of size. 39 In that study, no measurements of outflow facility were conducted. Here, we have used a particle that is smaller (90 nm diameter), in about 1000 × higher concentration (10 8 p.f.u.…”

Section: Adenoviral Particles (Arrows) Appear In Close Association Wimentioning

confidence: 97%