Signs of early damage in glaucomatous monkey eyes: Low spatial frequency losses in the pattern ERG and VEP

Marx, Marcia S.; Podos, Steven M.; Bódis-Wollner, Iván; Lee, Ping-Yu; Wang, Ron-Fang; Severin, C

doi:10.1016/s0014-4835(88)80075-7

Cited by 63 publications

(22 citation statements)

References 19 publications

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“…In particular, the PERG amplitude reduction observed in some patients with elevated intraocular pressure raises the possibility that PERG abnormalities may reflect early changes in visual function prior to the development of overt clinical signs of glaucoma. The observation that PERG abnormalities precede optic nerve damage in animal models of glaucoma [21] reinforces this suggestion, but the relationship of these deficits to the development of glaucoma remains unclear. In this study we attempted to determine whether unilateral reduction of IOP in individuals with ocular hypertension is associated with preservation of the response in the corresponding eye.…”

Section: Discussionmentioning

confidence: 81%

Steady-state pattern electroretinogram following long term unilateral administration of timolol to ocular hypertensive subjects

et al. 1990

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To determine whether long-term reduction of intraocular pressure leads to a corresponding preservation of the pattern electroretinogram (PERG), PERGs were studied in 21 patients with ocular hypertension who had received unilateral timolol therapy for a minimum of 6 years. The mean difference in intraocular pressure (IOP) between the placebo-treated and the timolol-treated eyes (over 6 years) was 2.4 mm Hg. Steady-state PERGs (16.0 rps) were obtained simultaneously in both eyes of each patient, with four check sizes (0.25, 0.5, 1.0 and 2.0 degrees). Significant (p less than 0.05) steady-state PERG deficits (i.e., amplitude more than two standard deviations below the mean value of age-matched controls) were observed in 16 eyes of 12 patients (10 placebo-treated and 6 timolol-treated eyes). The mean PERG amplitude did not differ significantly between the placebo-treated and timolol-treated eyes. However, a significant correlation (r = -0.423) in the IOP differences between the placebo-treated and timolol-treated eyes and the corresponding PERG amplitude differences was noted in three of the four test conditions (i.e. 0.25, 0.5, and 1.0 degrees). These results suggest that reducing IOP may preserve ganglion cell function in some patients with ocular hypertension.

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Section: Discussionmentioning

confidence: 81%

Steady-state pattern electroretinogram following long term unilateral administration of timolol to ocular hypertensive subjects

et al. 1990

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“…In this rodent glaucoma model, there is no apparent involvement of a compromised ocular blood¯ow, yet the ERG pathophysiology involving a-and b-wave amplitude reductions and lengthening of the b-wave implicit time is qualitatively similar to that found in the rat. On the basis of this similarity, we conclude that the predominantly rod-retina of rodents responds signi®-cantly differently than the primate retina does to chronic elevated IOP (Marx et al, 1988), and that close comparisons for similarity of the pathophysiology in the two types of retinas may not be warranted despite the fact that cones make up a small percentage of the rodent retina. Because mice and rats have traditionally been characterized as having`roddominated' retinas, and because signals originating in cone photoreceptors are so important in human vision, concern has been expressed that the mouse and the rat may be inadequate models for investigation of the retinal processing of cone signals.…”

Section: Discussionmentioning

confidence: 89%

Electroretinographic Abnormalities in a Rat Glaucoma Model with Chronic Elevated Intraocular Pressure

Bayer

Danias

Brodie

et al. 2001

Experimental Eye Research

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“…The changes to the optic nerve head in cynomolgus monkeys following argon laser-induced ocular hypertension are similar to those in human eyes with glaucoma (Radius & Pederson, 1984;Marx et al, 1988). The intraocular pressure of unilateral, ocular hypertensive, cynomolgus monkeys is decreased by the acute (Lee et al, 1985) and repeated instillation (Lee et al, 1987) of a range of clinically used ocular hypotensive agents.…”

Section: Intraocular Pressure Studiesmentioning

confidence: 64%

L‐662,583 is a topically effective ocular hypotensive carbonic anhydrase inhibitor in experimental animals

Sugrue

Gautheron²,

Mallorga

et al. 1990

British J Pharmacology

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1 L-662,583 was a potent inhibitor in vitro of purified, human erythrocyte carbonic anhydrase II, pos-sessing an IC50 of 0.7 nm. The IC50 values for MK-927, acetazolamide and methazolamide were 13.0 nm, 10.8 nm and 21.2 nm, respectively. 2 A 1 h pretreatment with one 50 u1 drop of a 0.1% solution of L-662,583 blocked carbonic anhydrase activity in a homogenate of the iris + ciliary body of albino rabbits by 63%. Similar treatment with 0.1% suspensions of acetazolamide and methazolamide elicited inhibitions of 30% and 20%, respectively. This ex vivo model indirectly assesses the ability of an agent to enter the rabbit eye. 3 Concentrations of L-662,583 in the cornea, aqueous humour and iris + ciliary body of albino rabbits were determined by h.p.l.c. at predetermined times after the instillation (one drop of 50pl) of a 2% solution of L-662,583. Peak levels for cornea (47.4pgg-1), aqueous humour (4.51 ygml-1) and iris + ciliary body (9.61 pgg 1-) occurred at 0.5, 2 and 1 h after instillation, respectively. 4 The experimentally elevated intraocular pressure of the right eye of rabbits, induced by prior intraocular injection of a-chymotrypsin, was maximally decreased by 4.5 mmHg, 6.2 mmHg and 9.8 mmHg after the instillation (one drop of 50pl) of 0.01%, 0.1% and 0.5% solutions of L-662,583, respectively. All three concentrations lowered intraocular pressure at all time points from 1 h up to and including 5 h, the last recorded time point. The unilateral instillation of L-662,583 (0.5%) into the contralateral, left eye failed to lower the elevated intraocular pressure of the untreated, right eye. This finding indicates that the site of action of topically applied L-662,583 in this paradigm is local. The ocular normotensive, albino rabbit was much less susceptible than the ocular hypertensive rabbit to the intraocular pressure lowering effect of topically applied L-662,583, with a 2% solution maximally decreasing intraocular pressure by 2.3 mmHg. 5 Unilateral ocular hypertension was elicited in the right eye of sedated, cynomolgus monkeys by argon laser-induced photocoagulation of the trabecular meshwork. The instillation (one drop of 50p1) of L-662, 583 (2%) significantly lowered the elevated intraocular pressure of the right eye at all time points from 1 h up to and including 5 h. The maximum decline was 8.3 mmHg at 3 h and this represented a reduction of 23% from the corresponding baseline value of 36.8 mmHg. The intraocular pressure of the hypertensive, right eye was maximally decreased by 4.1 mmHg and 4.8 mmHg after the instillation of 0.5% and 1% solutions of L-662,583, respectively. Like the rabbit, the normotensive eye of cynomolgus monkeys was more resistant than the hypertensive eye to the ocular hypotensive action of L-662, 583, as indicated by the inability of 0.5% and 1% solutions of the agent to lower intraocular pressure. L-662,583 (2%) maximally reduced the intraocular pressure of normotensive monkey eyes by 2.4 mmHg at 2 h. 6 L-662,583 is structurally different from MK-927, a carbonic anhydrase inhibit...

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Signs of early damage in glaucomatous monkey eyes: Low spatial frequency losses in the pattern ERG and VEP

Cited by 63 publications

References 19 publications

Steady-state pattern electroretinogram following long term unilateral administration of timolol to ocular hypertensive subjects

Steady-state pattern electroretinogram following long term unilateral administration of timolol to ocular hypertensive subjects

Electroretinographic Abnormalities in a Rat Glaucoma Model with Chronic Elevated Intraocular Pressure

L‐662,583 is a topically effective ocular hypotensive carbonic anhydrase inhibitor in experimental animals

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