A new method and device to induce transient retinal ischemia in the rat

Li, Bing; Pang, Iok‐Hou; Barnes, George; McLaughlin, Marsha A.; Holt, William F.

doi:10.1076/ceyr.24.6.458.8596

Cited by 14 publications

(5 citation statements)

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“…8,9 This minimally invasive technique employed the concept of oculopression to produce elevated IOP. [10][11][12] An advantage of the suture compression model is that it is not associated with ocular tissue penetration or traumatization, and therefore relatively preserves the immune privilege of the eye. It was reported that a mild, chronic IOP elevation was induced for at least 15 weeks following an initial IOP spike that appeared immediately after suture placement.…”

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confidence: 99%

A Mouse Model of Chronic Ocular Hypertension Induced by Circumlimbal Suture

Liu

Flanagan

2017

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. To develop a chronic ocular hypertension mouse model by inducing intraocular pressure (IOP) elevation using a suture technique previously developed for rats.METHODS. C57BL/6 mice were given monocular circumlimbal suture (10/0) placement under anesthesia (ketamine/xylazine). The suture was left in place for 12 weeks (n ¼ 10). A control group had the same treatment while it was removed after day 1 (n ¼ 10). Intraocular pressure, electroretinogram (ERG), and optical coherence tomography (OCT) were measured in both groups for 12 weeks. At week 12, animals were euthanized and retina was harvested for histologic assessment.RESULTS. In the group with extended suture placement, IOP spiked from 14.3 6 0.9 to 48.4 6 4.8 mm Hg immediately after suture implantation. At day 1, it declined to 33.2 6 3.7 mm Hg and remained elevated for 12 weeks. In the suture removal group, IOP normalized to baseline within a day following suture removal. In the group with prolonged IOP elevation, the retinal ganglion cell (RGC) mediated ERG responses continued to exacerbate and were significantly reduced by week 12 (P < 0.001). Progressive loss of retinal nerve fiber layer was found and it became significant from week 4 (P < 0.001). At week 12, significant loss of RGCs (P < 0.001) was noted. In the IOP normalization group, no alteration in ERG, OCT, and RGC counting was observed.CONCLUSIONS. The circumlimbal suture approach produces a mild chronic IOP elevation in mice. Functional and structural changes under model induction are largely independent of the initial IOP spike.Keywords: glaucoma, intraocular pressure, electroretinogram, optical coherence tomography, ganglion cell G laucoma is a chronic ocular disease, which is characterized by selective retinal ganglion cell (RGC) degeneration and progressive visual field loss. Elevated intraocular pressure (IOP) is a critical risk factor for disease development, and IOP lowering is the mainstay of disease management. [1][2][3] Over the past few decades, a variety of rodent models have been developed to simulate human glaucoma. [4][5][6][7] These models aim to induce either acute or chronic ocular hypertension leading to glaucomatous-like changes. By using such models, investigators have made significant insights into understanding the pathogenesis of the disease.Previously, a rat model of chronic IOP elevation using conjunctival circumlimbal suture was developed. 8,9 This minimally invasive technique employed the concept of oculopression to produce elevated IOP. [10][11][12] An advantage of the suture compression model is that it is not associated with ocular tissue penetration or traumatization, and therefore relatively preserves the immune privilege of the eye. It was reported that a mild, chronic IOP elevation was induced for at least 15 weeks following an initial IOP spike that appeared immediately after suture placement. Progressive loss of RGC function, retinal nerve fiber layer (RNFL) defect, and eventual cell death in the ganglion cell layer were observed under model induction, ...

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A Mouse Model of Chronic Ocular Hypertension Induced by Circumlimbal Suture

Liu

Flanagan

2017

Invest. Ophthalmol. Vis. Sci.

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“…The decrease may have been due to brief transient ischemia in the control eye or to stress related to the mechanical puncture, to which both eyes were subjected. Indeed, Li et al (2002) showed a decrease in the a-wave amplitude following 5 min of ischemic preconditioning. The increase of the a-wave amplitude on days 3 and 7 PI could not be ascribed to a decrease in the b-wave amplitude because it appeared only on day 3 when the b-wave had already undergone partial recovery.…”

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confidence: 97%

Monitoring the effect of mild ischemia with a built-in light-emitting diode contact lens electrode and a low-cost custom-made apparatus

Fleischman¹,

Parvari²,

Oron³

et al. 2012

Physiol. Meas.

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Electroretinography (ERG) is widely used in clinical work and research to assess the retinal function. We evaluated an easy to build ERG setup adapted for small animals comprising two contact lens electrodes with a built-in light-emitting diode and a custom-made amplification system. The system's sensitivity was tested by monitoring ERG in albino rat eyes subjected to mild ischemia. Flash ERG was recorded by two contact lens electrodes positioned on the rat's corneas and used alternately as test or reference. The a- and b-wave amplitudes, a-wave latency, b-wave implicit time and oscillatory potentials (OPs) were analyzed. Ischemia was achieved by elevating the intraocular pressure in the eye's anterior chamber. ERG was recorded on post-ischemia (PI) days -1, 1, 3 and 7. Morphological changes were analyzed on hematoxylin/eosin stained 5 µm sections of control 7d PI retinas. In control eyes, ERG exhibited a pattern similar to a standard recording. Retinas subjected to mild ischemia preserved ordered layered morphology, exhibiting approximately 30% loss of ganglion cells and no changes in gross morphology. By day 3 PI, ischemia caused an increase in the a-wave amplitude (from 34.9 ± 2.7 to 45.4 ± 4.3 µV), a decrease in the b-wave amplitude (from 248 ± 13 to 162 ± 8 µV), an increase in a-wave latency (from 11.1 ± 0.3 to 17.3 ± 1.4 ms) and b-wave implicit time (from 81.0 ± 1.6 to 90.0 ± 2.5 ms), and attenuation of OPs. The described setup proved sensitive and reliable for evaluating subtle changes in the retinal function in small animals.

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“…One of the major methods is retinal or ophthalmic artery ligation with temporary sutures (5,7,11). The other is mechanical pressure on the eye to increase IOP with a number of techniques (3,16). Our model simulates (or one-to-one corresponds with) increased IOP by elevation of the infusion bottle to control the intraoperative bleeding in pars plana vitrectomy.…”

Section: Discussionmentioning

confidence: 99%

A Short Duration Transient Ischemia Induces Apoptosis in Retinal Layers: An Experimental Study in Rabbits

Güreli̇k

Akyürek

et al. 2005

European Journal of Ophthalmology

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Purpose To investigate retinal cell apoptosis in an experimental transient, short duration ocular ischemia model. Methods An experimental ischemia model, which simulates creating temporary high intraocular pressure to control intraocular bleeding during pars plana vitrectomy, was set up. Rabbits were randomly divided into three groups. Group 1 was the control group. In Group 2, intraocular pressure was increased to 97 mmHg for 5 minutes. In Group 3, intraocular pressure was increased to 97 mmHg for 10 minutes. After 24 hours, terminal deoxyribonucleotidyl transferase-mediated dUTP-digoxigenin nick-end labeling assay was used to detect retinal apoptosis in rabbit eyes. Only nuclear staining in retinal cells was counted. Results Groups with 5 minutes and 10 minutes of ischemia showed significantly higher amount of ganglion cell layer apoptosis when compared with the control group (p<0.05). Light microscopy and standard hematoxylin-eosin did not show any significant damage in the retina cells. Conclusions Apoptotic cell death in the retinal cell layers occurs in temporary ischemia-reperfusion as early as 5 and 10 minutes duration.

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A new method and device to induce transient retinal ischemia in the rat

Abstract: The pulley method is an easy, non-invasive, and highly reproducible technique for inducing retinal ischemia in rats. This procedure may provide a useful animal model of ischemic retinopathy.

Cited by 14 publications

References 10 publications

A Mouse Model of Chronic Ocular Hypertension Induced by Circumlimbal Suture

A Mouse Model of Chronic Ocular Hypertension Induced by Circumlimbal Suture

Monitoring the effect of mild ischemia with a built-in light-emitting diode contact lens electrode and a low-cost custom-made apparatus

A Short Duration Transient Ischemia Induces Apoptosis in Retinal Layers: An Experimental Study in Rabbits

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