Purpose: To establish an experimental model of ocular hypertension in the mouse.
Methods: Twenty-two black Swiss mice were used. After anesthesia and pupil dilation, the anterior chamber was flattened by the aspiration of aqueous humor. Laser photocoagulation (532-nm wavelength, 200-mW power, 0.05-second duration, 200- micro m spot size) then was performed at the limbus. Intraocular pressure (IOP) was measured weekly for 4 weeks and biweekly for 12 weeks, by a microneedle method. Slit lamp biomicroscopy was performed throughout the period and the structural changes were assessed histologically. A treatment response was considered to be a success if either the mean of IOP measurements collected during the first 4 weeks was increased by 30% or more, or the mean of all measurements collected during the 12 week study period was increased by 30% or more.
Results: Laser-treated eyes showed significantly higher IOP than control eyes from 1 to 6 weeks (P < 0.001). The average IOP in treated eyes during the first 4 and 12 weeks was significantly higher than the control IOP (P < 0.001). These IOP increases were 7.1 and 3.8 mm Hg, respectively. During the first 4 weeks, sustained elevation of IOP was obtained in 64% (14/22) of the treated eyes. During the entire 12-week study, increased IOP was successfully maintained in 37% (7/19) of the treated eyes. After 6 weeks, elevated IOP often returned to normal or several mm Hg below normal. Histologic analysis at the end of the 12-week study showed no inflammatory cells in the anterior segment and confirmed that the angle was closed by the laser photocoagulation treatment.
Conclusions: This method produces persistent IOP elevation in mouse eyes and may be a promising experimental model for the investigation of the biological mechanisms of glaucomatous optic neuropathy.