Glaucoma drops control intraocular pressure and protect optic nerves in a rat model of glaucoma

John Morrison, Kristina B. Nylander, Andreas (Andy) Lauer, William O. Cepurna, Elaine Johnson

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Abstract

PURPOSE. To determine whether chronic topical glaucoma therapy can control intraocular pressure (IOP) and protect nerve fibers in a rat model of pressure-induced optic nerve damage. METHODS. Sixteen adult Brown Norway rats were administered unilateral episcleral vein injections of hypertonic saline to produce scarring of the aqueous humor outflow pathways. Twice daily applications of either artificial tears (n = 6), 0.5% betaxolol (n = 5), or 0.5%, apraclonidine (n = 5) were delivered to both eyes, and awake pressures were monitored with a TonoPen XL tonometer for 17 days before the rats were killed. RESULTS. For animals administered artificial tears, the mean IOP of the experimental eyes was 39 ± 2 mm Hg compared with 29 ± 1 mm Hg for the control eyes. This difference was statistically significant (P <0.001). Mean IOPs in the experimental eyes of animals administered betaxolol and apraclonidine were 29 ± 7 and 29 ± 4 mm Hg, respectively, whereas the mean IOP in the control eyes was 28 ± 1 mm Hg for both groups. There was no statistically significant difference among these values. The mean IOP for the experimental eyes in the betaxolol and apraclonidine groups was lower than that in animals administered artificial tears (P = 0.003). Quantitative histologic analysis of optic nerve damage in experimental eyes showed that four of the six animals administered artificial tears had damage involving 100% of the neural area. This degree of damage appeared in only 3 of 10 animals administered glaucoma therapy. Optic nerve protection was closely correlated with IOP history because damage was limited to less than 10% of the cross-sectional area in all animals in which the maximal lOP was less than or equal to 39 mm Hg, more than 2 SD below the mean value for eyes administered artificial tears. CONCLUSIONS. Topical glaucoma therapy in this model can prevent IOP elevation and protect optic nerve fibers.

Original languageEnglish (US)
Pages (from-to)526-531
Number of pages6
JournalInvestigative Ophthalmology and Visual Science
Volume39
Issue number3
StatePublished - Mar 1998

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Optic Nerve
Intraocular Pressure
Glaucoma
Betaxolol
Nerve Fibers
Pressure
Aqueous Humor
Cicatrix
Veins
Therapeutics
Lubricant Eye Drops
Injections
apraclonidine

ASJC Scopus subject areas

  • Ophthalmology

Cite this

Glaucoma drops control intraocular pressure and protect optic nerves in a rat model of glaucoma. / Morrison, John; Nylander, Kristina B.; Lauer, Andreas (Andy); Cepurna, William O.; Johnson, Elaine.

In: Investigative Ophthalmology and Visual Science, Vol. 39, No. 3, 03.1998, p. 526-531.

Research output: Contribution to journalArticle

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abstract = "PURPOSE. To determine whether chronic topical glaucoma therapy can control intraocular pressure (IOP) and protect nerve fibers in a rat model of pressure-induced optic nerve damage. METHODS. Sixteen adult Brown Norway rats were administered unilateral episcleral vein injections of hypertonic saline to produce scarring of the aqueous humor outflow pathways. Twice daily applications of either artificial tears (n = 6), 0.5{\%} betaxolol (n = 5), or 0.5{\%}, apraclonidine (n = 5) were delivered to both eyes, and awake pressures were monitored with a TonoPen XL tonometer for 17 days before the rats were killed. RESULTS. For animals administered artificial tears, the mean IOP of the experimental eyes was 39 ± 2 mm Hg compared with 29 ± 1 mm Hg for the control eyes. This difference was statistically significant (P <0.001). Mean IOPs in the experimental eyes of animals administered betaxolol and apraclonidine were 29 ± 7 and 29 ± 4 mm Hg, respectively, whereas the mean IOP in the control eyes was 28 ± 1 mm Hg for both groups. There was no statistically significant difference among these values. The mean IOP for the experimental eyes in the betaxolol and apraclonidine groups was lower than that in animals administered artificial tears (P = 0.003). Quantitative histologic analysis of optic nerve damage in experimental eyes showed that four of the six animals administered artificial tears had damage involving 100{\%} of the neural area. This degree of damage appeared in only 3 of 10 animals administered glaucoma therapy. Optic nerve protection was closely correlated with IOP history because damage was limited to less than 10{\%} of the cross-sectional area in all animals in which the maximal lOP was less than or equal to 39 mm Hg, more than 2 SD below the mean value for eyes administered artificial tears. CONCLUSIONS. Topical glaucoma therapy in this model can prevent IOP elevation and protect optic nerve fibers.",
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N2 - PURPOSE. To determine whether chronic topical glaucoma therapy can control intraocular pressure (IOP) and protect nerve fibers in a rat model of pressure-induced optic nerve damage. METHODS. Sixteen adult Brown Norway rats were administered unilateral episcleral vein injections of hypertonic saline to produce scarring of the aqueous humor outflow pathways. Twice daily applications of either artificial tears (n = 6), 0.5% betaxolol (n = 5), or 0.5%, apraclonidine (n = 5) were delivered to both eyes, and awake pressures were monitored with a TonoPen XL tonometer for 17 days before the rats were killed. RESULTS. For animals administered artificial tears, the mean IOP of the experimental eyes was 39 ± 2 mm Hg compared with 29 ± 1 mm Hg for the control eyes. This difference was statistically significant (P <0.001). Mean IOPs in the experimental eyes of animals administered betaxolol and apraclonidine were 29 ± 7 and 29 ± 4 mm Hg, respectively, whereas the mean IOP in the control eyes was 28 ± 1 mm Hg for both groups. There was no statistically significant difference among these values. The mean IOP for the experimental eyes in the betaxolol and apraclonidine groups was lower than that in animals administered artificial tears (P = 0.003). Quantitative histologic analysis of optic nerve damage in experimental eyes showed that four of the six animals administered artificial tears had damage involving 100% of the neural area. This degree of damage appeared in only 3 of 10 animals administered glaucoma therapy. Optic nerve protection was closely correlated with IOP history because damage was limited to less than 10% of the cross-sectional area in all animals in which the maximal lOP was less than or equal to 39 mm Hg, more than 2 SD below the mean value for eyes administered artificial tears. CONCLUSIONS. Topical glaucoma therapy in this model can prevent IOP elevation and protect optic nerve fibers.

AB - PURPOSE. To determine whether chronic topical glaucoma therapy can control intraocular pressure (IOP) and protect nerve fibers in a rat model of pressure-induced optic nerve damage. METHODS. Sixteen adult Brown Norway rats were administered unilateral episcleral vein injections of hypertonic saline to produce scarring of the aqueous humor outflow pathways. Twice daily applications of either artificial tears (n = 6), 0.5% betaxolol (n = 5), or 0.5%, apraclonidine (n = 5) were delivered to both eyes, and awake pressures were monitored with a TonoPen XL tonometer for 17 days before the rats were killed. RESULTS. For animals administered artificial tears, the mean IOP of the experimental eyes was 39 ± 2 mm Hg compared with 29 ± 1 mm Hg for the control eyes. This difference was statistically significant (P <0.001). Mean IOPs in the experimental eyes of animals administered betaxolol and apraclonidine were 29 ± 7 and 29 ± 4 mm Hg, respectively, whereas the mean IOP in the control eyes was 28 ± 1 mm Hg for both groups. There was no statistically significant difference among these values. The mean IOP for the experimental eyes in the betaxolol and apraclonidine groups was lower than that in animals administered artificial tears (P = 0.003). Quantitative histologic analysis of optic nerve damage in experimental eyes showed that four of the six animals administered artificial tears had damage involving 100% of the neural area. This degree of damage appeared in only 3 of 10 animals administered glaucoma therapy. Optic nerve protection was closely correlated with IOP history because damage was limited to less than 10% of the cross-sectional area in all animals in which the maximal lOP was less than or equal to 39 mm Hg, more than 2 SD below the mean value for eyes administered artificial tears. CONCLUSIONS. Topical glaucoma therapy in this model can prevent IOP elevation and protect optic nerve fibers.

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