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Editors Selection IGR 9-4
Anatomical structures: Outflow pathways
Comment by Daniel Stamer on:
58977 Anatomic changes in Schlemm's canal and collector channels in normal and primary open-angle glaucoma eyes using low and high perfusion pressures, Hann CR; Vercnocke AJ; Bentley MD et al., Investigative Ophthalmology and Visual Science, 2014; 55: 5834-5841
Resistance generation by the conventional outflow tissues sets intraocular pressure (IOP). While a great deal of progress has been made towards better understanding the regulation of resistance by the trabecular meshwork, little attention has been paid to resistance control distal to the inner wall of Schlemm's canal; where 25-50% of total outflow resistance is generated. Using micro-CT imaging of human eyes from normal and primary open-angle glaucoma (POAG) donors, Hann et al. compared anatomic changes in Schlemm's canal (SC) and collector channels (CC) of eyes subjected to normal and elevated perfusion pressures.
It is important to know whether drugs that soften conventional outflow tissues like rho kinase inhibitors restore function of valvelike collector channel ostia.
In response to an IOP of 20 mmHg (elevated), results show that SC volume and CC orifice area of normal eyes decreased, while the number of observable CCs significantly increased by 26%. In contrast, the number of observable CCs did not change in POAG eyes perfused at 20 mmHg. Moreover, there were a significantly greater number of CC occlusions observed in POAG versus normal eyes at elevated IOP. These parameters were not different between normal and POAG eyes perfused at 10 mmHg.
The investigators hypothesize that as SC collapses at elevated IOPs, a reserve population of CCs is mechanically exposed, acting like a relief valve. In POAG, such a compensatory mechanism may be diminished or lost due to stiffness and/or architectural changes in conventional outflow tissue properties associated with disease. These ideas are supported by data from other laboratories, and if true add to the number of dynamic pressure-dependent processes that work together in the conventional outflow tract to maintain intraocular pressure within a narrow range over a lifetime. Looking forward, it would be interesting to attempt visualization of these valve-like structures in real time, and explore strategies to restore their functionality in POAG. Equally important is to know whether drugs that soften conventional outflow tissues like rho kinase inhibitors restore function of these valve-like CC ostia.
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