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Kayla Ficarrotta; Effect of intracranial pressure on conventional outflow facility in rats. Invest. Ophthalmol. Vis. Sci. 2018;59(9):3479.
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© ARVO (1962-2015); The Authors (2016-present)
The contribution of intracranial pressure (ICP) to glaucoma has garnered renewed interest as strain in the optic nerve head depends not solely on intraocular pressure (IOP), but on the translaminar pressure gradient (TLPG), which is the difference between IOP and ICP. Studies have shown that ICP manipulation can have a marked impact on optic disc cupping and posterior eye health, suggesting that aberrant TLPG may play a role in normal tension glaucoma. Possible effects of ICP on the anterior eye are unknown. The purpose of this study was to examine whether ICP manipulation alters aqueous outflow physiology in rats.
The lateral ventricle of anesthetized, adult Brown-Norway rats was cannulated with a 25G needle and connected to a saline-filled reservoir and pressure sensor. The anterior chamber was then cannulated with a 33G needle and connected to a programmable syringe pump filled with artificial aqueous humor and a pressure sensor. Conventional outflow facility (C) was measured via a modified constant-pressure perfusion technique at baseline ICP and approximately 15 mmHg above baseline ICP.
C was 0.022 ± 0.004 µl/min/mmHg (n=10) in anesthetized rats at baseline ICP. Following ICP elevation, C was reduced by 40.5 ± 14.6 % (n=8); and the reduction was statistically significant in every animal. To assess the physiological origin of this effect, the animal was euthanized and outflow facility was measured again at elevated ICP. C was reduced by only 12.8 ± 12.0 (n=7) following death. In some experiments, tetrodotoxin (TTX) was topically administered to the eye of anesthetized animals exposed to elevated ICP. C was reduced by only 19.9 ± 11.4 % (n=2) in the presence of TTX, suggesting that the effect has a neural component. Mean arterial pressure did not significantly change following elevation of ICP (n=2).
Elevating ICP reduces the conventional outflow facility of rat eyes without changing mean arterial pressure. Facility is restored towards normal levels upon death or TTX application, suggesting the presence of a neural feedback mechanism that may serve to regulate the TLPG. Such a mechanism would provide as a new potential target for glaucoma therapies.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.
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