CAJ | 학술논문

目的观察复方卡波姆诱导的兔眼慢性高眼压模型前房角结构的改变特征.方法实验研究.将32只青紫蓝兔随机平均分为8组,分别对其左眼前房内注射0.3%复方卡波姆0.3 ml,对药物诱发的高眼压模型进行观察;再于术后1、2、3、4、6、8、10及12周分别随机处死一组兔,制作眼球标本,观察兔眼的前房角结构变化.结果随药物诱导时间的延长,兔眼压缓慢升高,高眼压持续时间约3个月.药物诱导后的前房角特征:早期以炎症反应为主,约3周后炎症反应减轻直至消失,4周后前房角以纤维变性为主,部分前房角粘连阻塞;电镜下观察可见角巩膜及葡萄膜处的小梁网扩张变形,轴心胶原和弹力样纤维增生;小梁内皮细胞与小梁带分离,分离的内皮细胞形似淋巴细胞且具有单核巨噬细胞样功能,吞噬的卡波姆颗粒通过Schlemm管内皮细胞的空泡转运;房水从管腔的内皮细胞大空泡数逐渐减少,出现裂孔现象;后期过多的卡波姆颗粒堆积于内皮细胞内,堵塞房水流出通道;诱导后晚期的模型眼前房角胶原增生,结构破坏.结论复方卡波姆诱导的兔眼慢性高眼压模型房水流出受阻的主要部位在小梁内皮网部.
목적 관찰복방잡파모유도적토안만성고안압모형전방각결구적개변특정.방법 실험연구.장32지청자람토수궤평균분위8조,분별대기좌안전방내주사0.3%복방잡파모0.3 ml,대약물유발적고안압모형진행관찰;재우술후1、2、3、4、6、8、10급12주분별수궤처사일조토,제작안구표본,관찰토안적전방각결구변화.결과 수약물유도시간적연장,토안압완만승고,고안압지속시간약3개월.약물유도후적전방각특정:조기이염증반응위주,약3주후염증반응감경직지소실,4주후전방각이섬유변성위주,부분전방각점련조새;전경하관찰가견각공막급포도막처적소량망확장변형,축심효원화탄력양섬유증생;소량내피세포여소량대분리,분리적내피세포형사림파세포차구유단핵거서세포양공능,탄서적잡파모과립통과Schlemm관내피세포적공포전운;방수종관강적내피세포대공포수축점감소,출현렬공현상;후기과다적잡파모과립퇴적우내피세포내,도새방수류출통도;유도후만기적모형안전방각효원증생,결구파배.결론 복방잡파모유도적토안만성고안압모형방수류출수조적주요부위재소량내피망부.
Objective To observe the anterior chamber angle changes occurred in compound Carbomer-induced chronic high intraocular pressure (IOP) model in rabbit eyes.Methods It was an experimental study.Thirty two rabbits were randomly divided into eight groups.Compound Carbomer (0.3%, 0.3 ml) was injected into the left anterior chamber.A group of rabbits were randomly killed after 1,2, 3, 4, 6, 8, 10 and 12 weeks.The anterior chamber of the rabbit eye specimens was observed.Results IOP increased slowly following the application of the drug, high IOP lasted for 3 months.The drug-induced changes of anterior chamber angle consisted of early inflammatory response and late fibrous changes.Inflammatory response occurred in early stage and reduced or disappeared after 3 weeks.Fibrous degeneration and adhesion obstruction occurred in the anterior chamber angle after 4 weeks.Under the electron microscope, the trabecular was expanded and deformed, with hyperplasia of collagen and elastic fibers.Endothelial cells were separated from the trabecular, and showed the morphology of lymphocytes,with the function similar to the macrophages.Phagocytized Carbomer particles were transported through the vacuoles of Schlemm's canal endothelial cells.Large vacuoles gradually reduced.Excessive Carbomer particles were accumulated in the endothelial cells and obstructed the Schlemm's canal.This induced the fibrous proliferation and the destruction of anterior chamber angle structures.Conclusions The obstruction of aqueous humor outflow induced by compound Carbomer in rabbit high IOP model is caused mainly by the changes in trabecular endothelial cells.