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Translimbal laser photocoagulation to the trabecular meshwork as a model of glaucoma in rats.
Invest Ophthalmol Vis Sci. 2002 Feb; 43(2):402-10.IO

Abstract

PURPOSE

To develop and characterize a model of pressure-induced optic neuropathy in rats.

METHODS

Experimental glaucoma was induced unilaterally in 174 Wistar rats, using a diode laser with wavelength of 532 nm aimed at the trabecular meshwork and episcleral veins (combination treatment group) or only at the trabecular meshwork (trabecular group) through the external limbus. Intraocular pressure (IOP) was measured by a tonometer in rats under ketamine-xylazine anesthesia. Possible retinal vascular compromise was evaluated by repeated fundus examinations and by histology. The degree of retinal ganglion cell (RGC) loss was assessed by a masked, semiautomated counting of optic nerve axons. Effects of laser treatment on anterior ocular structures and retina were judged by light microscopy.

RESULTS

After the laser treatment, IOP was increased in all eyes to higher than the normal mean IOP of 19.4 +/- 2.1 mm Hg (270 eyes). Peak IOP was 49.0 +/- 6.1 mm Hg (n = 108) in the combination group that was treated by a laser setting of 0.7 seconds and 0.4 W and 34.0 +/- 5.7 mm Hg (n = 46) in the trabecular group. Mean IOP after 6 weeks was 25.5 +/- 2.9 mm Hg in glaucomatous eyes in the combination group compared with 22.0 +/- 1.8 mm Hg in the trabecular group. IOP in the glaucomatous eyes was typically higher than in the control eyes for at least 3 weeks. In the combination group, RGC loss was 16.1% +/- 14.4% at 1 week (n = 8, P = 0.01), 59.7% +/- 25.7% at 6 weeks (n = 88, P < 0.001), and 70.9% +/- 23.6% at 9 weeks (n = 12, P < 0.001). The trabecular group had mean axonal loss of 19.1% +/- 14.0% at 3 weeks (n = 9, P = 0.004) and 24.3% +/- 20.2% at 6 weeks (n = 25, P < 0.001), increasing to 48.4% +/- 32.8% at 9 weeks (n = 12, P < 0.001). Laser treatment led to closure of intertrabecular spaces and the major outflow channel. The retina and choroid were normal by ophthalmoscopy at all times after treatment. Light microscopic examination showed only loss of RGCs and their nerve fibers.

CONCLUSIONS

Increased IOP caused by a laser injury to the trabecular meshwork represents a useful and efficient model of experimental glaucoma in rats.

Links

Publisher Full Text

Authors+Show Affiliations

Levkovitch-Verbin H
Glaucoma Research Laboratory, Wilmer Ophthalmological Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA.
Quigley HA
No affiliation info available
Martin KR
No affiliation info available
Valenta D
No affiliation info available
Baumrind LA
No affiliation info available
Pease ME
No affiliation info available

MeSH

AnimalsAxonsCell CountChronic DiseaseDisease Models, AnimalGlaucomaIntraocular PressureLaser CoagulationLimbus CorneaeOcular HypertensionOptic Nerve DiseasesRatsRats, WistarRetinal Ganglion CellsTrabecular Meshwork

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

11818384

Citation

Levkovitch-Verbin, Hana, et al. "Translimbal Laser Photocoagulation to the Trabecular Meshwork as a Model of Glaucoma in Rats." Investigative Ophthalmology & Visual Science, vol. 43, no. 2, 2002, pp. 402-10.
Levkovitch-Verbin H, Quigley HA, Martin KR, et al. Translimbal laser photocoagulation to the trabecular meshwork as a model of glaucoma in rats. Invest Ophthalmol Vis Sci. 2002;43(2):402-10.
Levkovitch-Verbin, H., Quigley, H. A., Martin, K. R., Valenta, D., Baumrind, L. A., & Pease, M. E. (2002). Translimbal laser photocoagulation to the trabecular meshwork as a model of glaucoma in rats. Investigative Ophthalmology & Visual Science, 43(2), 402-10.
Levkovitch-Verbin H, et al. Translimbal Laser Photocoagulation to the Trabecular Meshwork as a Model of Glaucoma in Rats. Invest Ophthalmol Vis Sci. 2002;43(2):402-10. PubMed PMID: 11818384.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Translimbal laser photocoagulation to the trabecular meshwork as a model of glaucoma in rats. AU - Levkovitch-Verbin,Hana, AU - Quigley,Harry A, AU - Martin,Keith R G, AU - Valenta,Danielle, AU - Baumrind,Lisa A, AU - Pease,Mary Ellen, PY - 2002/1/31/pubmed PY - 2002/2/15/medline PY - 2002/1/31/entrez SP - 402 EP - 10 JF - Investigative ophthalmology & visual science JO - Invest Ophthalmol Vis Sci VL - 43 IS - 2 N2 - PURPOSE: To develop and characterize a model of pressure-induced optic neuropathy in rats. METHODS: Experimental glaucoma was induced unilaterally in 174 Wistar rats, using a diode laser with wavelength of 532 nm aimed at the trabecular meshwork and episcleral veins (combination treatment group) or only at the trabecular meshwork (trabecular group) through the external limbus. Intraocular pressure (IOP) was measured by a tonometer in rats under ketamine-xylazine anesthesia. Possible retinal vascular compromise was evaluated by repeated fundus examinations and by histology. The degree of retinal ganglion cell (RGC) loss was assessed by a masked, semiautomated counting of optic nerve axons. Effects of laser treatment on anterior ocular structures and retina were judged by light microscopy. RESULTS: After the laser treatment, IOP was increased in all eyes to higher than the normal mean IOP of 19.4 +/- 2.1 mm Hg (270 eyes). Peak IOP was 49.0 +/- 6.1 mm Hg (n = 108) in the combination group that was treated by a laser setting of 0.7 seconds and 0.4 W and 34.0 +/- 5.7 mm Hg (n = 46) in the trabecular group. Mean IOP after 6 weeks was 25.5 +/- 2.9 mm Hg in glaucomatous eyes in the combination group compared with 22.0 +/- 1.8 mm Hg in the trabecular group. IOP in the glaucomatous eyes was typically higher than in the control eyes for at least 3 weeks. In the combination group, RGC loss was 16.1% +/- 14.4% at 1 week (n = 8, P = 0.01), 59.7% +/- 25.7% at 6 weeks (n = 88, P < 0.001), and 70.9% +/- 23.6% at 9 weeks (n = 12, P < 0.001). The trabecular group had mean axonal loss of 19.1% +/- 14.0% at 3 weeks (n = 9, P = 0.004) and 24.3% +/- 20.2% at 6 weeks (n = 25, P < 0.001), increasing to 48.4% +/- 32.8% at 9 weeks (n = 12, P < 0.001). Laser treatment led to closure of intertrabecular spaces and the major outflow channel. The retina and choroid were normal by ophthalmoscopy at all times after treatment. Light microscopic examination showed only loss of RGCs and their nerve fibers. CONCLUSIONS: Increased IOP caused by a laser injury to the trabecular meshwork represents a useful and efficient model of experimental glaucoma in rats. SN - 0146-0404 UR - https://www.unboundmedicine.com/medline/citation/11818384/Translimbal_laser_photocoagulation_to_the_trabecular_meshwork_as_a_model_of_glaucoma_in_rats_ L2 - https://iovs.arvojournals.org/article.aspx?volume=43&amp;issue=2&amp;page=402 DB - PRIME DP - Unbound Medicine ER -