A Novel Rabbit Model of Angle-Closure Glaucoma Via Ciliary Block and Elevated Trans-Lens Pressure Difference.

PURPOSE

Angle closure is a hallmark of primary angle-closure glaucoma (PACG), but the upstream biomechanical drivers initiating this process remain poorly understood. It has been recently proposed that ciliary block elevates the trans-lens pressure difference, initiating anterior chamber shallowing. However, this mechanism lacks direct in vivo validation. To address this gap, we established and characterized a novel rabbit model of angle-closure glaucoma induced by ciliary block-mediated trans-lens pressure difference.

METHODS

Thirty rabbits were divided into three groups: intraocular lens with a capsular tension ring (IOL+CTR), IOL only, and untreated control (n = 10 each). Ciliary block was induced in the IOL+CTR group via extracapsular lens extraction and implantation of an oversized (13-mm) CTR. Over 8 weeks, we monitored intraocular pressure (IOP), anterior chamber dynamics, and trans-lens pressure differences using tonometry and manometry, followed by histopathological evaluation.

RESULTS

The IOL+CTR group developed sustained ocular hypertension, with a significant trans-lens pressure gradient. Multivariate analysis identified this gradient as the potential primary driver of prominent anterior chamber shallowing and angle closure, features absent in the IOL and control groups. Consequently, the IOL+CTR animals exhibited classic glaucomatous optic neuropathy, characterized by a 50% reduction in retinal nerve fiber layer thickness and a markedly excavated optic nerve head. Furthermore, progressive exophthalmos occurred in 80% of these animals.

CONCLUSIONS

We successfully developed a reproducible rabbit model in which ciliary block-induced trans-lens pressure difference acts as a pivotal mechanistic link to anterior chamber shallowing, angle closure, and sustained IOP elevation, recapitulating key features of human angle-closure glaucoma.