Glaucoma drops control intraocular pressure and protect optic nerves in a rat model of glaucoma.
OBJECTIVE
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 IOP 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.
Morrison
J C
JC
Kenneth C. Swan Ocular Neurobiology Laboratory, Casey Eye Institute, Oregon Health Sciences University, Portland 97201, USA.
Nylander
K B
KB
Lauer
A K
AK
Cepurna
W O
WO
Johnson
E
E
D000316:Adrenergic alpha-Agonists / Q000008:administration & dosage*; D000319:Adrenergic beta-Antagonists / Q000008:administration & dosage*; D000818:Animals; D015784:Betaxolol / Q000008:administration & dosage*; D003000:Clonidine / Q000008:administration & dosage / Q000031:analogs & derivatives*; D004195:Disease Models, Animal; D005901:Glaucoma / Q000188:drug therapy* / Q000209:etiology / Q000473:pathology; D007429:Intraocular Pressure / Q000187:drug effects*; D008297:Male; D009412:Nerve Fibers / Q000187:drug effects / Q000473:pathology; D009798:Ocular Hypertension / Q000150:complications; D009883:Ophthalmic Solutions; D009900:Optic Nerve / Q000187:drug effects / Q000473:pathology; D009901:Optic Nerve Diseases / Q000209:etiology / Q000473:pathology / Q000517:prevention & control*; D051381:Rats; D011914:Rats, Inbred BN; D014065:Tonometry, Ocular
D000316:Adrenergic alpha-Agonists; D000319:Adrenergic beta-Antagonists; D009883:Ophthalmic Solutions; C016986:apraclonidine; D003000:Clonidine; D015784:Betaxolol