Pressure-Induced Retinal Ischemia in Rats: An Experimental Model for Quantitative Study

Büchi, Ernst R.; Suivaizdis, Irena; Fu, Jun

doi:10.1159/000310240

Cited by 151 publications

(96 citation statements)

References 11 publications

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“…1,11,12 Therefore, in the present study, we used the elevated IOP model to test the hypothesis that acute retinal ischemia via elevation of IOP can lead to endothelial dysfunction and impair vasodilation by reducing NO bioavailability through enhanced levels of superoxide. To eliminate the confounding effects (i.e., neural/glial and hemodynamic factors) commonly encountered in in-vivo preparations, we used an From the…”

Section: -15mentioning

confidence: 99%

“…[11][12][13][14][15] This model creates retinal ischemia by elevating and maintaining IOP above the retinal perfusion pressure, and correlates with the human diseases of acute angle-closure glaucoma, central retinal artery occlusion, and ophthalmic artery occlusion. 1,11,12 Therefore, in the present study, we used the elevated IOP model to test the hypothesis that acute retinal ischemia via elevation of IOP can lead to endothelial dysfunction and impair vasodilation by reducing NO bioavailability through enhanced levels of superoxide.…”

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confidence: 99%

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Acute Retinal Ischemia Inhibits Endothelium-Dependent Nitric Oxide–Mediated Dilation of Retinal Arterioles via Enhanced Superoxide Production

Hein¹,

Ren²,

Potts

et al. 2012

Invest. Ophthalmol. Vis. Sci.

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PURPOSE.Because retinal vascular disease is associated with ischemia and increased oxidative stress, the vasodilator function of retinal arterioles was examined after retinal ischemia induced by elevated intraocular pressure (IOP). The role of superoxide anions in the development of vascular dysfunction was assessed. METHODS. IOP was increased and maintained at 80 to 90 mm Hg for 30, 60, or 90 minutes by infusing saline into the anterior chamber of a porcine eye. The fellow eye with normal IOP (10 -20 mm Hg) served as control. In some pigs, superoxide dismutase mimetic TEMPOL (1 mM) or vehicle (saline) was injected intravitreally before IOP elevation. After enucleation, retinal arterioles were isolated and pressurized without flow for functional analysis by recording diameter changes using videomicroscopic techniques. Dihydroethidium (DHE) was used to detect superoxide production in isolated retinal arterioles. RESULTS. Isolated retinal arterioles developed stable basal tone and the vasodilations to endothelium-dependent nitric oxide (NO)-mediated agonists bradykinin and L-lactate were significantly reduced only by 90 minutes of ischemia. However, vasodilation to endothelium-independent NO donor sodium nitroprusside was unaffected after all time periods of ischemia. DHE staining showed that 90 minutes of ischemia significantly increased superoxide levels in retinal arterioles. Intravitreal injection of membrane-permeable radical scavenger but not vehicle before ischemia prevented elevation of vascular superoxide and preserved bradykinin-induced dilation. CONCLUSIONS. Endothelium-dependent NO-mediated dilation of retinal arterioles is impaired by 90 minutes of ischemia induced by elevated IOP. The inhibitory effect appears to be mediated by the alteration of NO signaling via vascular superoxide. T he neural retina tissue in patients exposed to acute periods of retinal ischemia suffers from blood flow deficit, which can lead to visual impairment and blindness.1,2 Ocular diseases and complications such as acute angle-closure glaucoma, retinal vascular occlusion, and elevated intraocular pressure during vitreous surgery or after vitreoretinal surgery, are associated with retinal ischemia.1-3 Currently, treatment modalities for restoring neural retina function are relatively limited. Experimental evidence demonstrating a reduction in retinal blood flow after the initial retinal ischemia suggests that dysfunction of arterioles, the major site for flow regulation, contributes to the persistent retinal damage. 4,5 However, studies are lacking to directly address whether vasomotor function of retinal arterioles is altered after acute retinal ischemia.In the retinal circulation, the vascular endothelium is important in regulating local blood flow by the release of vasoactive factors such as the potent vasodilator nitric oxide (NO) 6 and vasoconstrictor endothelin-1. 7 It has been shown in pigs that endothelium-dependent arterial dilation and release of NO surrounding the retinal arterioles are reduced in vivo after acute ...

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confidence: 99%

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confidence: 99%

Acute Retinal Ischemia Inhibits Endothelium-Dependent Nitric Oxide–Mediated Dilation of Retinal Arterioles via Enhanced Superoxide Production

Hein¹,

Ren²,

Potts

et al. 2012

Invest. Ophthalmol. Vis. Sci.

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“…In the ischemic group, the I/R injury model was developed using the method previously described by Buchi et al (12) . According to this method, to establish retinal ischemia, the right anterior chamber was cannulated with a 30-gauge needle attached to an infusion set, and its reservoir was placed approximately 200 cm above the animal.…”

Section: Methodsmentioning

confidence: 99%

Quercetin protects the retina by reducing apoptosis due to ischemia-reperfusion injury in a rat model

Arıkan¹,

Erşan²,

Karaca³

et al. 2015

Arquivos Brasileiros De Oftalmologia

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Purpose: This study aimed to investigate the effect of quercetin on apoptotic cell death induced by ischemia-reperfusion (I/R) injury in the rat retina. Methods: Twenty-four rats were divided into four equal groups: control, ischemic, solvent, and quercetin. I/R injury was achieved by elevating the intraocular pressure above the perfusion pressure. Intraperitoneal injections of 20 mg/kg of quercetin and dimethyl sulfoxide (DMSO) were performed in the quercetin and solvent groups, respectively, immediately prior to I/R injury, and the researchers allowed for the retinas to be reperfused. Forty-eight hours after injury, the thicknesses of the retinal ganglion cell layer (RGCL), inner nuclear layer (INL), inner plexiform layer (IPL), outer plexiform layer (OPL), and outer nuclear layer (ONL) were measured in all groups. Moreover, the numbers of terminal deoxynucleotidyl transferase dUTP nick-end-labeled [TUNEL (+)] cells and caspase-3 (+) cells in both INL and ONL were evaluated in all groups. Results: The administration of quercetin was found to reduce the thinning of all retinal layers. The mean thickness of INL in the quercetin and ischemic groups was 21 ± 5.6 µm and 16 ± 6.4 µm, respectively (P<0.05). Similarly, the mean thickness of ONL in the quercetin and ischemic groups was 50 ± 12.8 µm and 40 ± 8.7 µm, respectively (P<0.05). The antiapoptotic effect of quercetin in terms of reducing the numbers of both TUNEL (+) cells and caspase-3 (+) cells was significant in INL. The mean number of TUNEL (+) cells in INL in the ischemic and quercetin groups was 476.8 ± 45.6/mm 2 and 238.72 ± 251/mm², respectively (P<0.005). The mean number of caspase-3 (+) cells in INL of ischemic and quercetin groups was 633.6 ± 38.7/mm 2 and 342.4 ± 36.1/mm 2 , respectively (P<0.001). Conclusion:The use of quercetin may be beneficial in the treatment of retinal I/R injury because of its antiapoptotic effect on the retinal layers, particularly in INL.

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“…The addition of liquid into the chamber increases the pressure within the eye and compresses the vasculature passing through the optic disc and supplying the retina . Blood contained within these vessels is thereby expelled, cutting off the supply to the retinal tissue [15,16] . Such an intervention can be accomplished via cannulation of the eye, which is then connected to an elevated pressure liquid reservoir, which increases IOP to the level of the reservoir.…”

Section: Animal Models Of Retinal Ischemiamentioning

confidence: 99%

What can we learn about stroke from retinal ischemia models?

D'Onofrio

Koeberle

2012

Acta Pharmacol Sin

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Retinal ischemia is a very useful model to study the impact of various cell death pathways, such as apoptosis and necrosis, in the ischemic retina. However, it is important to note that the retina is formed as an outpouching of the diencephalon and is part of the central nervous system. As such, the cell death pathways initiated in response to ischemic damage in the retina reflect those found in other areas of the central nervous system undergoing similar trauma. The retina is also more accessible than other areas of the central nervous system, thus making it a simpler model to work with and study. By utilizing the retinal model, we can greatly increase our knowledge of the cell death processes initiated by ischemia which lead to degeneration in the central nervous system. This paper examines work that has been done so far to characterize various aspects of cell death in the retinal ischemia model, such as various pathways which are activated, and the role neurotrophic factors, and discusses how these are relevant to the treatment of ischemic damage in both the retina and the greater central nervous system.

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Pressure-Induced Retinal Ischemia in Rats: An Experimental Model for Quantitative Study

Cited by 151 publications

References 11 publications

Acute Retinal Ischemia Inhibits Endothelium-Dependent Nitric Oxide–Mediated Dilation of Retinal Arterioles via Enhanced Superoxide Production

Acute Retinal Ischemia Inhibits Endothelium-Dependent Nitric Oxide–Mediated Dilation of Retinal Arterioles via Enhanced Superoxide Production

Quercetin protects the retina by reducing apoptosis due to ischemia-reperfusion injury in a rat model

What can we learn about stroke from retinal ischemia models?

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