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Yasushi Wada, Tomomi Higashide, Kimikazu Sakaguchi, Atushi Nagata, Kazuyuki Hirooka, Kazuhisa Sugiyama; Correlation between decreased optic nerve head blood flow and retinal ganglion cell loss caused by systemically administrated aldosterone in rats. Invest. Ophthalmol. Vis. Sci. 2019;60(9):5629.
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© ARVO (1962-2015); The Authors (2016-present)
Impaired ocular blood flow may be one of the risk factors unrelated to the intraocular pressure (IOP) for the onset and progression of glaucoma. In previous reports the systemic administration of aldosterone decrease the number of retinal ganglion cells (RGCs) without an elevation of IOP. However, the mechanism of RGC loss in this particular animal model remains unknown. In this study, we investigated the optic nerve head (ONH) blood flow and retinal ganglion cell loss after systemic administration of aldosterone in rats.
Male Brown-Norway rats, 20 weeks of age, were administered an 80μg/kg/day dose of aldosterone or saline using an osmotic minipump implanted in the dorsum of the neck (n = 7 each). Before and 1, 2, and 4 weeks after aldosterone administration, ONH blood flow in the right eye, with the pupil dilated by 0.4% tropicamide, was evaluated under general anesthesia with the mean blur rate (MBR) measured by Laser speckle flowgraphy. MBR was separately determined in the vessel region (MV) and the tissue region (MT). Intraocular pressure (IOP), blood pressure, ocular perfusion pressure (OPP), and heart rate were also recorded at each time point. The number of retrogradely labeled RGCs were counted in the retinal flatmounts at 5weeks after systemic administration of aldosterone or saline (n = 4 each).
MV in the aldosterone-treated rats significantly decreased from baseline 2 and 4 weeks after administration (both p < 0.001), and MT significantly decreased from baseline at 2- week post-administration (p = 0.01). MV in the saline-treated rats significantly increased from baseline 2 weeks after administration (p = 0.02). MV and MT in the saline-treated rats were significantly higher than those in the aldosterone-treated rats (MV: 2 and 4 weeks, p <0.001, p = 0.002, respectively; MT: 2 weeks, p = 0.009). There were no significant changes in IOP, blood pressure, or OPP in both groups. RGCs significantly decreased in the aldosterone-treated rats compared to the saline-treated rats (p=0.003). MV and MT at 4 weeks were well correlated with the number of RGCs in both groups (MV: r = 0.77, p = 0.023; MT: r = 0.84, p = 0.009).
The systemic administration of aldosterone decreased ONH blood flow in rats and the decrease was closely related to RGC loss.
This abstract was presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 - May 2, 2019.
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