PURPOSE: To determine the role played by nitric oxide (NO) in the autoregulation of circulation in the optic nerve head (ONH). METHODS: The intraocular pressure (IOP) was increased and maintained at 50 mm Hg by the infusion of balanced saline solution (BSS) into the anterior chamber of albino rabbits. Experiments were performed with or without an intravenous injection of 10, 20, or 50 mg/kg N(G)-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase (NOS) inhibitor. The blood flow in the ONH was evaluated by the hydrogen clearance method, and NO metabolites (nitrite and nitrate) were measured in the ONH under the same experimental conditions in other rabbits. Visual evoked potentials (VEPs) were recorded before the IOP elevation and every 15 minutes during the 60 minutes of elevation. The effect of elevated IOP on the VEPs and the hemodynamics and NO levels in the ONH were determined. The effect of pretreatment with a NOS inhibitor on the IOP-induced changes was also investigated. RESULTS: The implicit time of the VEP was prolonged after L-NAME in a dose-dependent manner, whereas the implicit time in the control group (saline) was less affected. Blood flow in the ONH was not reduced by an elevation of the IOP (50 mm Hg) but was significantly reduced by L-NAME (20 mg/kg). The NO metabolites, which were elevated in the ONH during IOP elevation in the control, were also depressed by L-NAME pretreatment. CONCLUSIONS: These results indicate that NO may play a role in the autoregulation of circulation in the ONH during elevated IOP. This would mean that NO provides some neuroprotection during an acute phase of ischemia in the ONH.
PURPOSE: To determine the role played by nitric oxide (NO) in the autoregulation of circulation in the optic nerve head (ONH). METHODS: The intraocular pressure (IOP) was increased and maintained at 50 mm Hg by the infusion of balanced saline solution (BSS) into the anterior chamber of albino rabbits. Experiments were performed with or without an intravenous injection of 10, 20, or 50 mg/kg N(G)-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase (NOS) inhibitor. The blood flow in the ONH was evaluated by the hydrogen clearance method, and NO metabolites (nitrite and nitrate) were measured in the ONH under the same experimental conditions in other rabbits. Visual evoked potentials (VEPs) were recorded before the IOP elevation and every 15 minutes during the 60 minutes of elevation. The effect of elevated IOP on the VEPs and the hemodynamics and NO levels in the ONH were determined. The effect of pretreatment with a NOS inhibitor on the IOP-induced changes was also investigated. RESULTS: The implicit time of the VEP was prolonged after L-NAME in a dose-dependent manner, whereas the implicit time in the control group (saline) was less affected. Blood flow in the ONH was not reduced by an elevation of the IOP (50 mm Hg) but was significantly reduced by L-NAME (20 mg/kg). The NO metabolites, which were elevated in the ONH during IOP elevation in the control, were also depressed by L-NAME pretreatment. CONCLUSIONS: These results indicate that NO may play a role in the autoregulation of circulation in the ONH during elevated IOP. This would mean that NO provides some neuroprotection during an acute phase of ischemia in the ONH.
Authors: Jo-Hsuan Wu; Rafaella C Penteado; Sasan Moghimi; Linda M Zangwill; James A Proudfoot; Robert N Weinreb Journal: J Glaucoma Date: 2021-09-01 Impact factor: 2.290
Authors: Agnes Boltz; Reinhard Told; Katarzyna J Napora; Stefan Palkovits; René M Werkmeister; Doreen Schmidl; Alina Popa-Cherecheanu; Gerhard Garhöfer; Leopold Schmetterer Journal: PLoS One Date: 2013-12-06 Impact factor: 3.240