Optometry and Vision Sciences - Research Publications

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    Response of the Rat Optic Nerve to Acute Intraocular and Intracranial Pressure Changes
    Zhao, D ; He, Z ; Van Koeverden, A ; Vingrys, AJ ; Wong, VHY ; Lim, JKH ; Nguyen, CTO ; Bui, BV ; Wang, N (Springer Singapore, 2019)
    Glaucoma is a neurodegenerative disease, characterized by the progressive death of retinal ganglion cells. Elevated intraocular pressure (IOP) is known to be an important risk factor for glaucoma; however, it is not the only force acting on the optic nerve. Intracranial pressure (ICP) also exerts an effect on the optic nerve head, effectively opposing the force applied by IOP. Indeed, this balance of forces creates a pressure gradient (or the translaminar pressure gradient) across the optic nerve head [1]. Increasingly it is thought that the pressure difference between IOP and ICP, the translaminar pressure (TLP), may be critical for the integrity of the retina and optic nerve [2], and thus ICP may be an important risk factor for glaucoma [2–6].
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    How ganglion cell responses to IOP elevation are impacted by blood pressure and intracranial pressure
    Bui, BV ; van Koeverden, A ; He, Z ; Vingrys, AJ ; Nguyen, CTO ; Zhao, D (Association for Research in Vision and Ophthalmology, 2019-07-01)
    Purpose : The extent to which blood pressure or intracranial pressure modifies ganglion cell responses to acute intraocular pressure (IOP) elevation incompletely understood. Using the electroretinogram (ERG) we measure ganglion cell mediated responses in rat retina, whilst acutely modifying IOP, BP and ICP in a systematic manner. We quantify the relationship between ganglion cell function and ocular perfusion pressure (BP - IOP) at low, normal and high ICP. Methods : Six groups of adult Long-Evans rats (n=7-11 eyes/group, total animals = 25) were anaesthetised (60:5mg/kg ketamine:xylazine) and underwent acute pressure modification. A femoral artery and vein were cannulated for blood pressure measurement and manipulation (sodium nitroprusside to lower and angiotensin II to elevate pressure). ICP was set to -5, 5 or 25 mmHg via a dual cannula (30G infusion needle inside a 23G measurement needle) placed into the lateral ventricle (-1.5mm from bregma, ±2mm from midline) on the ipsilateral side to the cannulated eye (30G, vitreal chamber). At each ICP (-5, 5 or 25 mmHg) and BP setting (normal or high), IOP was raised from 10 to 90 mmHg in 10 mmHg steps (3 min each). At each IOP level ganglion cell function was assessed using the scotopic threshold response (-5 log cd.s/m2, 20 repeats). Data were compared using one- and two-way ANOVA. Results : Average blood pressure at baseline was similar for the normal blood pressure groups (ICP-5 93±3; ICP5 99±5; ICP25 105±3mmHg, p=0.8). There was significant BP elevation in all the high blood pressure groups (ICP-5 160±3; ICP5 157±3; ICP25 157±5mmHg p<0.001). Compared with normal blood pressure groups (32.0±2.0μV), animals with high blood pressure (24.5±1.8μV) had significantly smaller baseline STR amplitudes (p<0.01). There was also a significant ICP effect (p<0.01), with larger baseline amplitudes in the 25mmHg ICP group (34.8±1.6μV) compared with normal (26.4±2.5μV) and low ICP groups (23.9±2.5μV). The ocular perfusion pressure (BP-IOP) relationship fully could not account for difference in ganglion cell function between ICP levels. Conclusions : Ganglion cell function is dependent on ocular perfusion pressure, excessive low or high perfusion attenuates function. Higher intracranial pressure appears to protect against acute ocular perfusion stress.