摘要
An experimental model of rhegmatogenous retinal detachment in rabbits was established to simulate the pathophysiologic condition of human RRD. 24 rabbits were randomly divided into 3 groups and underwent vitrectomy with a vitrector and/or retinotomy with a Charles flute needle, with 12 in group Ⅰ (vitrectomy and retinotomy), 7 in group Ⅱ (retinotomy) and 5 in group Ⅲ (vitrectomy). All animals underwent follow-up examinations with direct and indirect ophthalmoscopy and fundus photography 12 h and day 1, 3, 5, 7, 10, 14, 21, and 28 after the procedure(s). Retinal changes were recorded. As a result, 10 RRDs were successfully established in group Ⅰ. Direct and indirect ophthalmoscopy and fundus photography demonstrated typical features of RRD. No RRD developed in group Ⅱ and Ⅲ. It was concluded that the experimental rhegmatogenous retinal detachment produced in a rabbit model after vitrectomy with retinotomy in this study was a convenient and reliable one. This RRD model mimicked the typical pathophysiological changes in humans.
An experimental model of rhegmatogenous retinal detachment in rabbits was established to simulate the pathophysiologic condition of human RRD. 24 rabbits were randomly divided into 3 groups and underwent vitrectomy with a vitrector and/or retinotomy with a Charles flute needle, with 12 in group Ⅰ (vitrectomy and retinotomy), 7 in group Ⅱ (retinotomy) and 5 in group Ⅲ (vitrectomy). All animals underwent follow-up examinations with direct and indirect ophthalmoscopy and fundus photography 12 h and day 1, 3, 5, 7, 10, 14, 21, and 28 after the procedure(s). Retinal changes were recorded. As a result, 10 RRDs were successfully established in group Ⅰ. Direct and indirect ophthalmoscopy and fundus photography demonstrated typical features of RRD. No RRD developed in group Ⅱ and Ⅲ. It was concluded that the experimental rhegmatogenous retinal detachment produced in a rabbit model after vitrectomy with retinotomy in this study was a convenient and reliable one. This RRD model mimicked the typical pathophysiological changes in humans.
