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L F Rosenberg, D P Karalekas, T Krupin, A Hyderi; Cyclocryotherpay and noncontact Nd:YAG laser cyclophotocoagulation in cats.. Invest. Ophthalmol. Vis. Sci. 1996;37(10):2029-2036.
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PURPOSE: To investigate physiological and histologic alterations of the cat eye in response to cyclocryotherapy (CCT) and noncontact transscleral Nd:YAG laser cyclophotocoagulation (TSNYC). METHODS: One eye of 29 cats was treated with 12 applications (1 minute, -80 degrees C) of CCT or 80 applications of noncontact TSNYC (7 to 9 J, retrofocus 3.6 mm). Blood-aqueous barrier function was studied measuring aqueous protein and fluorescein concentration after intravenous dye injection. Ocular blood flow was determined using 85Sr microspheres. RESULTS: Intraocular pressure after CCT was 29% lower in the treated than in the control eye after 3 and 12 weeks. After TSNYC, pressure was reduced by 34% at 3 weeks and by 27% after 12 weeks. Aqueous protein concentration was elevated in all treated eyes. Neither technique altered tonographic outflow facility or episcleral venous pressure. Calculated aqueous flow was lower in the treated eye than in the control eye 3 and 12 weeks after each cyclodestructive procedure. After CCT, anterior chamber fluorescein concentration was 2.5 times greater in 3-week and 3 times greater in 12-week eyes. After TSNYC, fluorescein concentration was 3 and 3.5 times greater at 3 and 12 weeks, respectively. Ciliary body blood flow in control eyes was similar to CCT and TSNYC eyes. Histopathology 12 weeks after CCT and TSNYC showed pigment dispersion, disorganized architecture, and cystic elevation of the nonpigmented ciliary epithelium. Areas of absent pigmented and nonpigmented epithelium at the ciliary process base were more discrete in TSNYC eyes. Electron microscopy demonstrated normal junctional complexes. CONCLUSIONS: CCT and TSNYC lower pressure by reducing aqueous formation. Ciliary body blood flow is not altered after either technique. Both techniques result in similar histologic disruption of the ciliary epithelium, resulting in breakdown of the blood-aqueous barrier.
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