玻璃体超微结构与玻璃体液化

玻璃体是眼球的主要组成部分,玻璃体液化在许多眼病的发病机制中起重要作用,但有关玻璃体的超微结构及玻璃体液化的机制知之甚少。了解玻璃体的结构组成,不仅能理解疾病的发病过程,而且有助于疾病的治疗。本就近年来在此方面的研究进展综述。     

玻璃体液化生物力学特性及临床研究进展

玻璃体液化是一种与年龄相关的退行性改变,随后会进一步影响玻璃体及其周围组织的理化性质,导致多种相关眼部疾病.玻璃体液化最主要的病理改变是透明质酸逐渐耗竭和胶原网状结构塌陷,其中伴随着一系列玻璃体生物力学特性的改变.因此,本文对正常眼玻璃体的生物力学特性、玻璃体生物力学特性的测量方法、玻璃体液化形成机制和生物力学特性的改变以及玻璃体液化与眼病的关系等进行综述,以期为将来有效地减缓和治疗玻璃体液化提供思路.     

玻璃体黄斑交界面疾病的研究进展

玻璃体黄斑牵引包括黄斑裂孔、黄斑前膜、玻璃体黄斑牵引综合征等.其发病机制尚不完全清楚.较公认的是玻璃体年龄相关性的改变及玻璃体视网膜界面细胞增生,产生玻璃体黄斑牵引即对黄斑区前后及切线方向的牵拉,引起复杂的病理变化.现今研究者开展的多途径实验研究,如手术标本光、电镜组织学观察,免疫组织学比较,细胞因子检测等发现此类疾病有各自特征.由此衍生出的各种发生机制假说成为新技术应用和治疗的根据,如某些药物作用于玻璃体或玻璃体黄斑界面以诱导玻璃体液化及玻璃体后脱离.     

白内障超声乳化术对玻璃体结构的影响

目的 :探讨超声乳化晶体摘除术后玻璃体凝胶结构的改变。方法 :新西兰白兔麻醉后以不同的超声乳化时间摘除晶体。超声乳化晶体摘除术后 1周将兔眼摘出 ,检测玻璃体的液化率。结果 :当超声乳化时间在 0、 0 5、 1 0、 2 0分钟时 ,玻璃体的液化率分别为 2 1 2± 4 8% ,2 5 8± 7 1% ,41 2± 8 2 %和 5 2 1± 11 5 %。超声乳化后玻璃体凝胶结构有较明显丧失。结论 :兔眼超声乳化摘除晶体后玻璃体凝胶结构随超声乳化时间增加而出现液化现象     

辅助性药物诱导玻璃体后脱离的研究进展

玻璃体视网膜交界面的状态与许多玻璃体视网膜疾病的发生发展密切相关.近年来研究表明,玻璃体切割术前应用药物可使玻璃体液化或使许多增生性玻璃体视网膜疾病玻璃体内的纤维增生膜溶解,解除玻璃体后皮质与视网膜内界膜之间的粘连,形成完全性玻璃体后脱离,不但有利于手术的进行而且有利于玻璃体视网膜疾病的治疗和视力的恢复.本文对目前药物诱导玻璃体后脱离的组织结构、药物的作用机制及其在临床和实验研究方面的进展作简要综述.     

玻璃体后脱离及其并发症的发病机制

在衰老过程中,玻璃体液化和玻璃体视网膜界面改变可诱发玻璃体后脱离(posterior vitreous detachment,PVD).不完全PVD及异常PVD通过玻璃体视网膜牵拉作用以及容量和化学转移可引起视网膜裂孔、孔源性视网膜脱离、视网膜前膜、黄斑水肿、年龄相关性黄斑变性、黄斑裂孔、玻璃体黄斑牵拉综合征等一系列并发症.为防止这些并发症进一步加重,减轻疾病恶化的风险,可以提前诱导完全性PVD或者采用玻璃体切除手术.目前药物性玻璃体融解术已进入临床前期研究,非酶试剂等非侵入性的治疗方法也在探索阶段.     

重新认识玻璃体的功能

随着对玻璃体越来越深入的研究,临床上需要重新认识一下玻璃体的功能,异常的玻璃体后脱离(posterior vitreous detachment,PVD)可以导致视网膜脱离、玻璃体黄斑牵拉综合征、黄斑裂孔等疾病,而在玻璃体液化或者缺失状态下,却容易罹患核性白内障及原发性开角型青光眼(primary open angle glaucoma,POAG).此外,研究还发现玻璃体可以调节氧含量及分布,从而使玻璃体液化对缺血性视网膜疾病可能有益.     

玻璃体视网膜界面早期变化的研究

在解剖上,玻璃体后皮质与视网膜相邻,玻璃体与视网膜的关系是既相互独立,又紧密联系的。病理状态时,玻璃体的改变为许多玻璃体视网膜疾病的发生、发展提供了一个良好的生长环境,玻璃体在许多玻璃体视网膜疾病的发生发展中起了关键性作用。消除玻璃体改变在疾病中的作用,是近年来眼科界极为关注的一个问题。本文通过对玻璃体和玻璃体视网膜交界面结构和黏连机制、玻璃体与视网膜界面变化的危险因素、对视网膜疾病影响的描述,阐述了玻璃体后脱离对玻璃体视网膜界面疾病的影响及采用的检测方法及意义。     

软骨素酶对兔眼玻璃体及玻璃体视网膜界面的影响

目的 探讨玻璃体腔内注射软骨素酶(CA)诱导产生玻璃体液化的能力及其对玻璃体视网膜界面黏附作用的影响。方法 36只新西兰白兔随机分成Ⅰ、Ⅱ、Ⅲ组，右眼为实验眼，各12眼，分别注射CA 0．1、0．2、1 U／0．1mL；左眼为对照眼，注射等量的平衡盐溶液(BSS)。于注射后不同时间行临床观察、电生理及组织病理学检查。结果 注射后1周，实验组兔眼即可观察到玻璃体液化，但未见玻璃体后脱离(PVD)。注射后5周，实验组全部兔眼玻璃体液化，部分兔眼发现临床可见的PVD并经组织学检查证实。对照组未见玻璃体液化及PVD。结论 CA能在较短的时间内诱导产生玻璃体液化并对玻璃体视网膜间粘连有一定的破坏作用。     

糖尿病玻璃体性状特点及其与增殖性糖尿病视网膜病变的关系

糖尿病患者体内持续的高血糖及相应的病理状态不仅会导致糖尿病视网膜病变(DR)，也会影响玻璃体代谢，导致糖尿病玻璃体病变。由于玻璃体与视网膜在解剖位置上毗邻，因此糖尿病玻璃体病变与DR在发生发展方面相互促进，特别是玻璃体后脱离(PVD)和玻璃体劈裂等玻璃体视网膜界面的改变，为纤维血管增殖膜的生长提供了支架，并与玻璃体切割术(PPV)术中操作密切相关。本文整理了糖尿病患者玻璃体结构及胶原交联产物改变、玻璃体视网膜界面改变及其与增殖性糖尿病视网膜病变(PDR)关系的相关研究，旨在深入了解糖尿病玻璃体病变，为DR的研究和治疗、PPV手术方案的制定等提供参考。     

Analysis of the vitreous membrane in a case of type 1 Stickler syndrome

Background  Stickler syndrome causes ocular abnormalities, including retinal detachment and vitreoretinal degeneration, and systemic anomalies such as arthritis and deafness. Although retinal detachment is characteristic of this syndrome, the pathogenesis is unknown. Case report  A 10-year-old boy reported decreased vision and presented 5 days after visual loss. Results  Ophthalmoscopy showed a retinal detachment with a giant tear in the right eye, and a nonpigmented epithelial detachment with pars plicata breaks in the left eye. Bilateral findings included an empty vitreous and a vitreous membrane at the equator. The systemic abnormalities included short stature and joint hypermobility. The diagnosis was type 1 Stickler syndrome, and the eyes were treated surgically. Immunohistochemistry showed that the vitreous membrane resected intraoperatively was comprised primarily of Müller cells. Electron microscopy showed dense collagen fibers around the cells in the membrane that were identical to the vitreous collagen inserted into the basement membrane of the cells, which was similar to the ultrastructure of the vitreous base. Conclusion  Müller cells might be primary components of the vitreous membrane in type 1 Stickler syndrome. The vitreoretinal interface, which resembled the ectopic vitreous base, in the vitreous membrane may be related to the pathogenesis of the retinal detachment.     

玻璃体后脱离与高度近视眼的研究进展

本文论述了玻璃体后脱离的病因和发病机制，分类和临床特点，并揭示了玻璃体后脱离与高度近视眼的关系。     

视网膜孔源性玻璃体出血23例临床分析

目的:探讨视网膜裂孔源性玻璃体出血的发病原因、临床特征和治疗效果。方法:收集了自发性玻璃体出血病例23眼,玻璃体出血原因均为马蹄形视网膜裂孔伴裂孔区血管撕裂所致,2眼为单纯视网膜裂孔并发玻璃体出血,21眼为孔源性视网膜脱离并发玻璃体出血;3眼行单纯激光治疗,20眼行外路视网膜脱离手术或玻璃体切除手术。结果:经激光或手术治疗后23眼均无出血复发,裂孔封闭,22眼视力好于或等于术前,1眼视网膜脱离复发为牵拉型视网膜脱离。结论:孔源性玻璃体出血是玻璃体积血的重要原因之一,尽早明确诊断、及时治疗可以取得满意疗效,避免严重并发症。     

Pharmacologic Vitreolysis

It is now well recognized that vitreous plays an important role in the pathogenesis of various retinal disorders. In many instances it can be addressed with pars plana vitrectomy, although this approach, like any surgery, has its limitations. The search for alternatives or adjunct to surgery has led to the development of pharmacologic vitreolysis. The use of intravitreal agents to alter the vitreous in order to reduce or eliminate its role in disease seems promising. The purpose of this article is to summarize the present knowledge on pharmacologic vitreolysis. A review of the different agents used and of ongoing trials will be presented. Also, current understanding of vitreous structure and its interaction with the retina will be discussed.     

实验性玻璃体腔内高氧对视网膜超微结构的影响

目的 通过研究玻璃体腔内高氧对视网膜超微结构的影响，观察氧对视网膜组织的毒性作用，为实现临床应用玻璃体腔内的氧疗提供基础实验依据。方法：以2个月龄猪为实验动物，模拟临床常规玻璃体切割手术后眼内充填混合气体，在混合气体中提高氧比例达40％，设置眼内充填常规混合气体组和空白对照组做为实验对照组，持续数天后观察视网膜全层超微结构的改变。结果 眼内高氧组7d即可引起视网膜神经节细胞核膜的明显溶解，双层膜结构消失，且导致胞浆内线粒体肿胀，双层膜结构模糊，嵴排列出现紊乱。结论 玻璃体腔内的氧含量增加到一定程度（40％）时，则可引起视网膜组织的氧化损害，具有一定的氧毒性。     

Vitreous function and intervention of it with vitrectomy and other modalities

The vitreous body, the largest intraocular component, plays a key role in eye development, refraction, cell barrier function, oxygen metabolism and the pathogenesis of assorted diseases. Age, refraction and systemic diseases can cause vitreous metabolic abnormalities. With the continuous development of vitrectomy techniques and equipment, vitreous injections and vitrectomies have increased over the recent decades. However, the normal oxygen tension gradient in the vitreous helps to protect the lens and anterior chamber angle from oxidative stress damage, whereas the increased vitreous oxygen tension around lens and the trabecular meshwork after vitrectomy. It may lead to postoperative nuclear cataract and increase the risk for glaucoma. As a conventional procedure, scleral buckling holds several advantages over vitrectomy in selected cases. This review raises concerns regarding the function of the vitreous and encourages conducting vitreous interventions prudently if it is possible.     

猪眼基底部玻璃体视网膜界面的超微结构观察

目的:观察离体猪眼玻璃体腔内注射酶后基底部玻璃体视网膜界面的超微结构。方法:取新鲜尸体猪眼130眼,随机均分A,B,C,D及对照组共5组,每组再分为2小组,每小组各13只。其中A和B组为透明质酸酶(hyaluronidase,HA)组,分别于玻璃体腔内注射终浓度为200,800U/mL的HA0.1mL;C和D组为软骨素酶(chondroitinase,CA)组,分别于玻璃体腔内注射终浓度为10,50U/mL的CA0.1mL;对照组玻璃体内注射磷酸缓冲盐(PBS)0.1mL。各组的眼球分别在37℃下水浴15min和30min后取出,经4%戊二醛和自配视网膜固定液固定,行石蜡切片苏木素-伊红染色检查、基底部扫描电镜检查及透射电镜检查,观察基底部玻璃体视网膜情况。结果:病理检查显示,大体标本和切片均见基底部玻璃体有部分液化、降解;扫描电镜显示,CA50U/mL组和HA800U/mL组均可见基底部玻璃体与对照组相比有显著减少;透射电镜显示,实验组(B,C,D组)各组玻璃体视网膜界面残余纤维较对照组明显减少。结论:体外使用HA和CA均可诱导猪眼基底部玻璃体脱离,但CA可能引起的眼内副作用更大。     

Vitreous substitutes:challenges and directions

Thenatural vitreous body has a fine structure and complex functions. The imitation of the natural vitreous body by vitreous substitutes is a challenging work for both researchers and ophthalmologists. Gases, silicone oil, heavy silicone oil and hydrogels, particularly the former two vitreous substitutes are clinically widely used with certain complications. Those, however, are not real artificial vitreous due to lack of structure and function like the natural vitreous body. This article reviews the situations, challenges, and future directions in the development of vitreous substitutes, particularly the experimental and clinical use of a new artificial foldable capsular vitreous body .     

葡萄膜炎的玻璃体手术治疗进展

葡萄膜炎是发生于眼内的一种炎性反应,是眼科常见的致盲疾病。目前国内外在其治疗上有一些研究和报道。我们分析了葡萄膜炎的病因及发病机制,对葡萄膜炎的玻璃体手术治疗进行归纳,现综述如下。     

Vitreomacular traction and exudative age‐related macular degeneration

Vitreomacular traction resulting from lacking, incomplete or anomalous posterior vitreous detachment is suspected to play a crucial role in the pathogenesis of different forms of age‐related macular degeneration (AMD) along with the known mechanisms. It is probable that the fundamental pathomechanisms of AMD formation have already begun by the time tractional forces lead to a change for the worse. Vitreomacular traction alone is perhaps not able to induce AMD. It would seem sensible to consider vitreous changes when diagnosing and treating AMD patients because of the high coincidence of vitreomacular traction and choroidal neovascularization (CNV) and the often successful treatment of other diseases of the vitreoretinal interface by vitrectomy. The concept of the pathogenesis of AMD should therefore be extended to include the influence of the vitreous, especially where therapeutic concepts such as pharmacological vitreolysis and vitreous separation have been established as causative treatment of late forms of AMD.