Effects of prostaglandin-mediated and cholinergic-mediated miosis on morphology of the ciliary cleft region in dogs

Abstract

OBJECTIVE To compare morphology of the ciliary cleft (CC) region in dogs after topical administration of latanoprost, pilocarpine, or a combination of latanoprost and pilocarpine. ANIMALS 6 Beagles. PROCEDURES A prospective 4-phase crossover study with washout periods was performed. Latanoprost (phase L), pilocarpine (phase P), pilocarpine followed by latanoprost (phase PL), and latanoprost followed by pilocarpine (phase LP) were administered to the right eye. Artificial tears were administered to the left eye (control eye). For each phase, pupil diameter and intraocular pressure (IOP) were measured and ultrasonographic biomicroscopy was performed 2 hours after topical treatment. Angle opening distance (AOD), ciliary cleft width (CCW), ciliary cleft length (CCL), and ciliary cleft area (CCA) were evaluated. RESULTS All treated eyes had marked miosis without significant differences in pupil diameter among phases. Significant IOP reductions were detected for all phases, except phase P. The AOD and CCA were significantly increased in all phases for treated eyes, compared with results for control eyes. The CCW was significantly increased in phases P, PL, and LP; CCL was significantly increased in phases PL and LP. Comparison of treated eyes among phases revealed that CCW differed significantly between phases L and P and between phases L and PL. CONCLUSIONS AND CLINICAL RELEVANCE Prostaglandin-mediated and cholinergic-mediated miosis caused variations in CC configurations. When latanoprost and pilocarpine were used in combination, the first drug administered determined the cleft morphology, which was not fully reversed by the second drug. The CC morphology did not fully explain IOP reductions.

Safety and efficacy of topically administered netarsudil‐latanoprost fixed dose combination (FDC; Rocklatan™) in normal and glaucomatous dogs with ADAMTS10‐open‐angle glaucoma (ADAMTS10‐OAG)

“…This treatment effect was more obvious in OAG‐affected dogs than in normal dogs and was consistent with previous reports describing the IOP effect of latanoprost and other prostaglandin analogues in these animals 14–16,32–34 . To the best of our knowledge, the underlying mechanism of latanoprost's treatment effects is believed to be a combination of increased uveoscleral and conventional aqueous humor outflow, the latter being facilitated by widening of the canine ciliary cleft via pupil constriction 35,36 …”

“…[14][15][16][32][33][34] To the best of our knowledge, the underlying mechanism of latanoprost's treatment effects is believed to be a combination of increased uveoscleral and conventional aqueous humor outflow, the latter being facilitated by widening of the canine ciliary cleft via pupil constriction. 35,36 We observed an obvious circadian treatment effect, especially with the q24h drug administration: Mean IOPs were highest at 8 a.m., 24 h after the last administration, and immediately before the next treatment. Following the eye drop administration at 8 a.m., mean IOPs were lower at the 11:30 a.m. and 3:30 p.m. time points.…”

Evaluation of ciliary cleft changes after phacoemulsification using ultrasound biomicroscopy in dogs with cataracts

“…Second, uveitis occurs in 90% of non-diabetic dogs immediately after phacoemulsification ( 1 , 32 ). Prostaglandin mediators produced in uveitis can affect CC parameters ( 33 , 34 ). One study reported that the incidence of CCA increased when latanoprost, a prostaglandin mediator, was used alone ( 33 ).…”

Ultrasound Biomicroscopy Studies to Evaluate Ciliary Cleft Parameters in Healthy Eyes of American Cocker Spaniels

“…The other ciliary cleft parameters, namely AOD, CCW, and CCA, are associated with its anatomic structure. In other words, if the ciliary cleft collapses, then these parameters also change (Sihota et al, 2005;Hasegawa and Kawata, 2015;Park et al, 2018). Inadequate assessment of structural changes within the ciliary cleft may prevent the early diagnosis of canine primary glaucoma (Hasegawa and Kawata, 2015).…”