氪离子黄光与红光联合治疗视网膜血管病致黄斑水肿

目的：分析氪离子黄光与红光联合光凝治疗视网膜血管病致黄斑水肿的临床效果。方法：对确诊黄斑弥漫性水肿与囊样水肿29例41只眼，包括糖尿病视网膜病变(diabetic retinopathy,DR)23例35只眼；视网膜静脉阻塞(retinal venous occlusion,RVO)6例6只眼采用氪离子黄光与红光联合光凝，对其效果进行分析。结果：41只眼术后1个月视力提高27只眼占65．8％；3个月视力提高37只眼占90．2％；6—12个月后随访到31只眼，其中5只眼发生玻璃体出血，其余26只眼中有24只眼视力提高占92．3％。术后3个月，黄斑水肿消退7只眼占17．1％；水肿明显减轻26只眼占63．4％；水肿无变化6只眼占14．6％；水肿加重2只眼占4．9％。结论：两种波长激光联合治疗视网膜血管病致黄斑水肿，可达到更有效的治疗目的。     

玻璃体内注射曲安奈德治疗黄斑水肿的 临床疗效观察

目的评价玻璃体内注射曲安奈德（TA）治疗黄斑水肿的疗效和安全性。方法符合入选条件的黄斑水肿患者37例41只眼，其中，视网膜静脉阻塞（RVO）组21例21只眼、糖尿病视网膜病变（DR）组13例17只眼、其他原因组3例3只眼。治疗前3组的平均视力分别为0.07、0.06、0.08。光相干断层扫描（OCT）检查显示，RVO组和DR组黄斑中心凹平均厚度分别为（974±394）、（873±213） μm。均采用 40 mg/ml 的TA 0.1 ml玻璃体内注射。用药后平均随访8个月，对比观察用药前后的视力、眼压、晶状体及眼底改变以及OCT检测的黄斑区视网膜厚度变化。结果41只眼中，除1只眼视力无变化外，其余眼视力均有不同程度提高。3组患者用药后6个月时随访，平均视力分别上升至0.25、0.20和0.35。全部治疗眼临床检查均显示黄斑水肿减轻或消退，OCT检查显示，RVO组和DR组治疗后1个月时，黄斑中心凹平均厚度分别为（173±41）、（204±76） μm。与治疗前比较，差异有统计学意义（t 值分别为8.323和6.842，P 值均 < 0.01）。6只眼眼压高于21 mm Hg（1 mm Hg=0.133 kPa），占146%。眼压升高发生于用药后1周至2个月，经局部用β受体阻滞剂眼压均能控制正常。1只眼白内障发展；另有1例糖尿病玻璃体切割手术后黄斑水肿患者，用药2个月后出现黄斑裂孔。RVO组和DR组中各有2只眼因黄斑水肿复发，在第一次用药后4~5个月再次玻璃体内注射TA 0.1 ml。结论玻璃体内注射TA对于常规治疗无效的黄斑水肿有一定疗效；一过性眼压升高是最常见的不良反应。尚需进一步评价其长期疗效和安全性。(中华眼底病杂志,2005,21:209-212)     

激光诱导脉络膜视网膜静脉吻合术对非缺血型视网膜静脉阻塞所致黄斑水肿的疗效观察

目的 观察激光诱导脉络膜视网膜静脉吻合术治疗非缺血型视网膜静脉阻塞（retinal vein occlusion,RVO）所致黄斑水肿的疗效。 方法 非缺血型RVO患者37例37只黄斑水肿眼均使用氪红激光诱导脉络膜视网膜静脉吻合，吻合术后随访6~12个月(平均随访9个月)，对比分析建立和未建立脉络膜视网膜静脉吻合的眼治疗前后视力、眼底、荧光素眼底血管造影（fundus fluorescein angoigraphy, FFA）、中心5°视网膜光敏感度的改变。 结果 37只眼中，激光治疗后2个月内有18只眼建立脉络膜视网膜静脉吻合，成功率48.6%。建立与未建立脉络膜视网膜静脉吻合的眼，治疗前后平均最佳矫正视力差异有显著性意义（P＜0.001）。建立吻合的眼，中心5°光敏感度与治疗前相比有明显提高（t=2.910, P＜0.005）；FFA显示16只眼黄斑水肿消失或减轻，2只眼黄斑囊样水肿仍存在。未建立吻合的眼，中心5°光敏感度与治疗前相比有所下降（t=1.928, P＜0.05），FFA显示黄斑水肿加重。 结论 RVO所致黄斑水肿未发展至囊样变性之前，激光诱导建立脉络膜视网膜静脉吻合可使RVO所致黄斑水肿消退或减轻，从而改善视功能。 （中华眼底病杂志，2002，18：10-12）     

玻璃体手术和眼内光凝治疗伴玻璃体积血和新生血管膜的视网膜静脉阻塞

目的评估玻璃体手术和眼内光凝治疗伴玻璃体积血、新生血管膜或牵拉性视网膜脱离的视网膜静脉阻塞(retinal vein occlusion,RVO)的疗效。方法复习连续的37例RVO患者经玻璃体手术和眼内光凝治疗的38只眼临床资料。视网膜分支静脉阻塞(branch retinal vein occlusion,BRVO)19例20只眼，视网膜中央静脉阻塞(central retinal vein occlusion,CRVO)18例18只眼。结果手术中确认27只眼有新生血管膜，23只眼有牵拉性视网膜脱离。手术后34只眼视力改善，占89.5%，其中22只眼有0.1以上的视力。4只眼视力未变。CRVO组病史较长，手术后视力改善较少。结论玻璃体手术和眼内光凝能改善多数伴有玻璃体积血、新生血管膜和牵拉性视网膜脱离的RVO眼预后。(中华眼底病杂志,1998,14:3-6)     

视网膜血管瘤分期及治疗效果观察

目的观察不同临床分期的视网膜血管瘤采用激光光凝、冷冻、玻璃体视网膜手术以及瘤体切除等方法治疗的临床效果，探讨玻璃体视网膜手术治疗的适应证 。方法回顾分析22例视网膜血管瘤33只患眼治疗前后的临床资料。治疗前按照视网膜血管瘤有无明显扩张供养血管、周围渗出、局限性视网膜脱离、广泛视网膜脱离至晚期并发症的过程,将本病分为5期。其中13只患眼主要采用单纯激光光凝治疗；5只 患眼主要采用冷冻联合激光光凝治疗；11只眼患眼采用玻璃体视网膜手术治疗，其中3只眼同时进行了视网膜血管瘤瘤体切除治疗。治疗后平均随访时间46个月，对比分析患者治疗前 后视力、视网膜血管瘤以及视网膜等情况。结果单纯激光光凝治疗的1 3只眼视网膜血管瘤均退行萎缩，视网膜平伏，视力提高2只眼，不变11只眼；冷冻联合激光光凝治疗的5只眼中，4只眼视网膜血管瘤退行萎缩，未见血管瘤复发，1只眼出现玻璃体视 网膜增生及玻璃体积血需进一步采用玻璃体视网膜手术治疗，视力提高2只眼，不变2只眼，下降1只眼；玻璃体视网膜手术治疗的11只眼中，1只眼出现新的血管瘤，2只眼血管瘤引起 渗出性视网膜脱离，2只眼再次出现玻璃体视网膜增生，8只眼视网膜平伏，视力提高3只眼，不变3只眼，下降5只眼。同时进行视网膜血管瘤瘤体切除治疗的3只眼中均未见血管瘤复发，2只眼视网膜平伏，1只眼出现渗出性视网膜脱离，视力提高2只眼，下降1只眼。结论单纯激光光凝或联合冷冻治疗对早期视网膜血管瘤患者有效；对伴有玻璃体积血、视网膜前膜形成、增生明显、视网膜脱离范围大的晚期视网膜血管瘤病变宜采用玻璃体视网膜手术治疗，视网膜血管瘤瘤体切除可有选择性应用，其远期效果仍有待观察。  （中华眼底病杂志，2008，24：107-110）     

非外伤性严重玻璃体积血主要病因回顾性分析

目的 观察非外伤性严重玻璃体积血患者的病因构成及变化趋势。方法 2005年1月至2011年12月行玻璃体切割手术治疗的非外伤性严重玻璃体积血患者1107例1202只眼纳入研究。按收治时间对患者进行分组,2005年1月至2008年12月为A组,2009年1月到2011年12月为B组。A组患者415例444只眼;B组患者692例758只眼。回顾分析引起玻璃体积血的病因构成及变化趋势。结果 A组444只眼中,视网膜静脉阻塞（RVO）156只眼、增生型糖尿病视网膜病变（PDR）117只眼、视网膜裂孔或脱离（RH／RD）61只眼、视网膜静脉周围炎（Eales 病）42只眼、渗出型老年性黄斑变性（EAMD）20只眼,占同期玻璃体积血患眼的89.19%;RVO患者比例最多。B 组758只眼中,PDR 347只眼、RH／RD 135只眼、RVO 133只眼、Eales病 29只眼、EAMD 22只眼,占同期玻璃体积血患眼的87.87%;PDR患者比例最多,RVO次之。PDR引起的玻璃体积血构成比逐年增加。结论 PDR、RVO、RH／RD、Eales 病、EAMD是非外伤性严重玻璃体积血的常见原因;PDR引起的玻璃体积血呈增加趋势。     

视网膜静脉阻塞激光治疗后玻璃体出血的临床分析

目的：了解视网膜静脉阻塞(RVO)激光治疗后发生玻璃体出血的原因。方法：回顾分析2年来门诊11例(11眼，CRVO：2眼；BRVO：9眼)激光后的视网膜静脉阻塞发生玻璃体出血的病例。结果：11例RVO中：少量玻璃体出血5例；中-多量玻璃体出血6例，其中2例作玻璃体切除术，其余激光治疗后出血停止而治愈。由初次激光治疗到玻璃体出血时间6月-11年，再次激光或／和手术后视力均有改善。结论：不规范或不完全的视网膜光凝是导致RVO激光治疗发生玻璃体出血的主要原因，规范的视网膜光凝、定期随诊和眼底荧光造影是保证疗效的关键。     

玻璃体手术后交感性眼炎的临床及病理学观察

目的观察玻璃体手术后交感性眼炎的临床特点及病理学改变。方法回顾性分析1998年1月至2004年12月期间13000例玻璃体手术后8例交感性眼炎患者的临床资料，并对其中3例摘除的诱发眼进行了病理学观察。结果交感性眼炎的发生率为0.06%。发生交感性眼炎的时间距最后一次玻璃体手术的时间为7~150 d，平均时间为(77.8±50.8) d。主要表现为交感眼视力下降、视物变形，眼红，眼痛。发病时交感眼视力为手动~0.5，诱发眼视力为无光感~0.04。双眼羊脂状角膜后沉着、前房闪辉及细胞、玻璃体混浊、视盘水肿充血、后极部视网膜水肿，2例交感眼有渗出性视网膜脱离。所有患者经口服泼尼松1.0~1.5 mg/kg治疗后交感眼和诱发眼视力均有不同程度恢复。3例患者因诱发眼视力丧失行眼球摘除手术。被摘除的诱发眼病理检查表现为葡萄膜弥漫性淋巴细胞浸润增厚，类上皮细胞结节形成，淋巴细胞浸润巩膜孔道，眼球萎缩。结论玻璃体手术后交感性眼炎发生率为0.06%；大多数发生在手术后3个月内；其临床表现及病理学检查符合交感性眼炎的特征。（中华眼底病杂志，2007，23：112-114）     

系统性红斑狼疮眼底病变25例临床分析

目的 探讨系统性红斑狼疮（SLE）眼底并发症的临床特点。 方法 回顾性分析25例出现眼底并发症的SLE患者的眼底、眼部其他表现、伴随的全身病变及血抗核抗体（ANA）、抗双链DNA（抗dsDNA）、补体3（C₃）、 补体4（C₄）和血红细胞沉降率(ESR)。 结果 “典型的”SLE眼底病变15例25只眼，视网膜静脉阻塞(RVO)9例12只眼，RVO合并视网膜动脉不全阻塞1例2只眼，渗出性视网膜脱离1例2只眼，玻璃体积血合并新生血管性青光眼1例1只眼，视盘水肿（除外RVO所 致）3例6只眼。9例合并有眼部其他表现，21例患者伴随有全身症状，所有病例血抗核抗体( ANA)、抗dsDN A阳性和血ESR升高，19例C₃下降，17例C₄下降。 结论 SLE可产生严重的 眼底并发症及合并其他眼部病变，对SLE患者应定期进行眼科检查，以便早期发现眼底病变 并及时进行治疗。 （中华眼底病杂志，2004，20：206-208）     

曲安奈德玻璃体腔注射治疗视网膜静脉阻塞和糖尿病视网膜病变继发黄斑水肿分析

目的 观察玻璃体腔注射曲安奈德(TA)治疗视网膜静脉阻塞(RVO)继发黄斑水肿和糖尿病性黄斑水肿的疗效以及二者疗效比较.方法 对经间接检眼镜、荧光素眼底血管造影(FFA)以及光学相干断层扫描(OCT)检查确诊的RVO继发黄斑水肿患者91例91只眼,其中中央视网膜静脉阻塞(CR-VO)55只眼(缺血型13只眼,非缺血型42只眼),分支视网膜静脉阻塞(BRVO)36只眼(缺血型10只眼,非缺血26眼).糖尿病性黄斑水肿患者67例73只眼,非增殖性糖尿病视网膜病变(PPDR)17只眼,增殖性糖尿病视网膜病变(PDR)56只眼,行TA玻璃体腔注射,治疗后随访3月至1年,对比分析术前术后的视力、眼底、FFA表现,观察OCT显示黄斑水肿高度.结果 最终随访RVO组视力提高者48只眼(52.7%),视力不变者39只眼(42.9%),视力下降者4只眼(4.40%).OCT形态恢复正常者50只眼(54.9%),改善者27只眼(29.7%),无改善者14只眼(15.4%).DR组视力提高者25(34.2%)只眼,,视力不变者45只眼(61.6%),视力下降者3只眼(4.11%).OCT形态恢复正常者24只眼(32.9%),改善者22只眼(30.1%),无改善者27只眼(37.0%).两组有效率行统计学分析,有显著性差异.RVO组24只眼术后出现一过性眼压升高,一眼白内障,一眼眼内炎,8只眼2次注射.DR组14眼术后出现一过性眼压升高,2只眼白内障,9只眼2次注射.结论 玻璃体腔注射TA是一种安全有效的治疗视网膜静脉阻塞继发黄斑水肿和糖尿病性黄斑水肿的方法,治疗视网膜静脉阻塞继发黄斑水肿的疗效好于糖尿病性黄斑水肿.     

Vitreous and macular diseases

We investigated the vitreous in its origin, morphology, metabolism and regeneration, and its role in various vitreomacular diseases. Focal vitreous liquefaction developed anterior to a laser induced chorioretinal scar in rabbit eyes, which suggested that a normal retina is necessary to maintain the integrity of the vitreous. We measured levels of hyaluronic acid and of the precursor of type II collagen in vitreous samples obtained by vitrectomy. Those levels declined with age in women. The precursor of type II collagen was at the same level in the samples from vitrectomy and those obtained by fluid air exchange, which suggested a persistent secretion of type II collagen into the vitreous cavity even after vitrectomy. We found a posterior precortical vitreous pocket in human autopsied eyes whose vitreous was stained with fluorescein. Using the same methods, we confirmed the presence of intravitreal fibrous membranes in the "tractus" in the anterior vitreous. In clinical studies using biomicroscopy, observations during surgery, scanning laser ophthalmoscopy, and optical coherence tomography (OCT), we clarified the role of premacular vitreous cortex which forms the posterior wall of the "pocket" in the premacular membrane and macular hole. The premacular vitreous cortex seems to be the main structure of the premacular membrane and its contraction may cause macular hole. Ring-shaped proliferation tends to develop along the outer margin of the "pocket". OCT demonstrated that some diabetic macular edema is caused by traction of the premacular vitreous cortex. Vitrectomy appear to be effective for diabetic macular edema by eliminating vitreous traction and the accumulated cytokine in the "pocket". The retina appears to have a program for vitreous metabolism throughout life, including the premacular pocket formation.     

Localisation of opticin in human proliferative retinal disease

This study sought to determine the distribution of opticin, an extracellular matrix small leucine-rich repeat protein secreted by the non-pigmented ciliary body epithelium (CBE), in pathological eye tissues including posterior hyaloid membranes (PHM) and epiretinal membranes (ERM) from subjects with proliferative diabetic retinopathy (PDR), central retinal vein occlusion (CRVO) and proliferative vitreoretinopathy (PVR). Eight enucleated eyes and eleven surgically excised PHMs/ERMs from patients with PDR, CRVO or PVR were analysed by immunohistochemistry for the presence and distribution of opticin, vitreous (delineated by a type II collagen antibody) and blood vessels (using CD31 and CD34 antibodies as endothelial markers). Opticin was present at the basal surface of the non-pigmented CBE and, in a patchy distribution, within CBE cells in all 8 enucleated globes. It also co-localised with the type II collagen of vitreous, where present, in these eyes. Opticin was present in 16 of the 19 PHMs/ERMs, where it was arranged in layers (10 membranes), diffusely (4 membranes) or in foci (2 membranes). Where in a layered pattern, opticin co-localised with vitreous type II collagen incorporated into the membrane, whereas the other two patterns did not co-localise with type II collagen labelling. We concluded that even in advanced proliferative retinal disease, the CBE continues to express and secrete opticin. Opticin was co-distributed with vitreous type II collagen and was also present in the pre-retinal membranes of proliferative retinopathies, where it could play a role in their development.     

Preservation of structure and immunoreactivity at the vitreoretinal interface of the rabbit eye

Background  The vitreous body is implicated in the etiology and pathology of a variety of retinal conditions. Many such conditions are treated surgically to remove the posterior vitreous from the inner limiting lamina (ILL) of the retina, and there is current interest in the adjunct use of enzymes for this purpose. To evaluate the efficacy of these agents in future preclinical studies, improved preservation and assessment methods were developed to establish a baseline histological profile of the vitreous and retina of the rabbit, to identify and distinguish artifactual vitreoretinal separation from authentic posterior vitreous detachment, and to preserve structural integrity while maintaining antigenicity for immunohistochemical analysis. Methods  Two pigmented rabbits each underwent perfusion with one of three fixatives, either: (1) 10% neutral buffered formalin + cetylpyridinium chloride (NBF/CPC), (2) acid-ethanolic formalin + CPC (AEF/CPC), or (3) formaldehyde-glutaraldehyde + CPC (FG/CPC). An eye fixed in NBF/CPC by immersion, from an additional rabbit, was also included for comparison. Eyes were processed whole through paraffin infiltration. Treatments were assessed by immunohistochemical labeling for retinal and cortical vitreous (CV) markers. Results  In contrast to immersion fixation, perfusion with either NBF/CPC or AEF/CPC maintained vitreous adherence to the ILL during histological processing. NBF/CPC proved best for highlighting intralaminar structure and for labeling type II collagen in the CV, particularly with antigen retrieval. AEF/CPC caused condensation of fibrillar elements in the CV. Collagen XVIII in the ILL was observed with AEF/CPC exclusively. Only retinal vessels near the optic nerve head were labeled for type IV collagen. The labeling of glia was useful for distinguishing between cellular and extracellular elements. GF/CPC hindered detection of collagen II and disrupted posterior segment structure. Expression of type II collagen extended from the ONH directly to CV affiliated with the central canal of Cloquet, a feature characteristic of rabbit eyes. Discussion  Careful tissue preservation and processing techniques minimize artifactual separation of the CV from the ILL. By optimizing the tissue architecture and antigenicity of the vitreoretinal complex, CV may be distinguished from the ILL immunohistochemically. The techniques described may be used to evaluate more effectively the utility of pharmacologic vitreolysis, using experimental animal models. Presented in part at the 2006 meeting of The Association for Research in Vision and Ophthalmology, Fort Lauderdale, Florida. This study was supported by Bausch & Lomb, Inc., with whom QualTek Molecular Laboratories has a contractual relationship. We had full control of all primary data, and we all agree to allow Graefe’s Archive for Clinical and Experimental Ophthalmology to review our data upon request.     

光化学法诱导兔视网膜静脉阻塞的实验研究

目的应用光化学法建立实验性兔视网膜静脉阻塞（retinal vein occlusion,RVO）模型。方法新西兰白兔10只,静脉注射孟加拉红后,激光照射视网膜静脉诱导兔眼RVO模型。分别于建模后1h、1d、3d行直接眼底镜和眼底荧光血管造影检查（fundus fluorescein angiography,FFA）。3d后摘除实验眼,行组织学检查。结果9只兔眼经光化学法诱导后,直接眼底镜、FFA检查见光凝远端视网膜静脉扩张迂曲、视网膜出血水肿等典型RVO表现;组织学检查证实光凝视网膜静脉有静脉血栓形成。结论应用光化学法能成功建立可复制、稳定的兔RVO模型,应用此动物模型,可进一步探索RVO的药物治疗并评价其疗效。     

玻璃体腔注射Avastin治疗眼底病400例临床疗效总结

目的:通过对400例眼底病患者520眼经玻璃体腔注射avastin治疗的临床疗效观察,说明玻璃体腔注射avastin对视网膜静脉阻塞(RVO)、糖尿病性视网膜病变(DR)、年龄相关性黄斑变性(ARMD)、中心性浆液性脉络膜视网膜病变(CSC)、视网膜脉络膜新生血管(CNV)等眼底病的治疗能起到重要的作用,并对其副作用作了总结分析统计。方法:对我院门诊确诊为RVO,DR,ARMD,CSC,CNV等眼底病患者400例眼底病患者520眼进行玻璃体腔注射avastin治疗,注射治疗1次/mo,以治疗前后的视力、眼底荧光血管造影(FFA)、眼压、光学相干断层扫描(OCT)作为观察指标,对经玻璃体腔注射avastin治疗的疗效进行分析总结;并对治疗过程当中出现的并发症作了总结、分析。结果:随访时间为3mo～1a,520眼中有467眼(89.8%)视力提高2行以上,眼压正常、视网膜水肿及出血明显吸收,新生血管消退,OCT及FFA指标都有好转;36眼(6.9%)视力稳定,治疗前后视力无变化,但眼底情况都有改善,无新生血管增生加重或眼压升高等并发症的发生;17眼(3.3%)视力下降,其中有13眼(2.5%)从0.2降至0.1,病变稳定;1眼(0.2%)发生了眼内炎,视力从0.6下降至0.2;1眼(0.2%)发生了视网膜中央动脉阻塞(CRAO),视力从0.02变为光感;1眼(0.2%)发生了玻璃体出血;1眼(0.2%)发生了孔源性视网膜脱离,伴有并发症而视力下降的患者中除了1眼(CRAO)外其余在对症治疗后视力均有提高;在所有的治疗眼中发生一过性眼压升高20眼(3.8%),后经降眼压对症治疗后眼压正常。还有1例患者右眼行玻璃体腔注射avastin治疗后3d左眼施行了小梁切除手术,术后切口愈合较一般手术后慢7～10d,眼压相对较低。结论:经玻璃体腔注射avastin治疗视RVO,DR,ARMD,CSC,CNV等眼底病,是一种有效、安全的方法,能提高视力,减轻黄斑和视网膜水肿,促进玻璃体和视网膜下出血的吸收,能有效地消退视网膜和脉络膜新生血管,可以抑制虹膜红变和新生血管性青光眼的发生;对于在治疗过程中出现的并发症也是值得我们去总结、思考的。     

玻璃体腔磁性液体对兔视网膜组织病理变化的初步研究

目的探讨玻璃体腔注射不同浓度磁性液体后,兔眼视网膜组织病理学变化情况。方法将18只健康新西兰大白兔,双眼玻璃体腔注射不同浓度磁性液体,其中右眼注射浓度为1％,左眼注射浓度为0．5％。分别于注射后1d、1周、1个月和3个月采用裂隙灯显微镜活体观察兔眼前节形态,并于注射后1周、1个月和3个月分别处死6只实验兔,制备视网膜铺片,经苏木精-伊红染色后观察视网膜组织结构的变化。结果裂隙灯显微镜检查：术后1d,所有术眼前房清亮,未见明显Tyndall征;术后3个月,所有术眼也未出现白内障。视网膜切片可见,术后1周时磁性物质分布于视网膜前,术后1个月和3个月时磁性物质有所减少,整个过程均未见明显的视网膜及视盘组织结构的水肿。结论光学显微镜下两种浓度的磁性液体对兔视网膜组织无明显损伤。     

A mouse model for Stickler's syndrome: ocular phenotype of mice carrying a targeted heterozygous inactivation of type II (pro)collagen gene (Col2a1)

The influences of targeted heterozygous inactivation of type II (pro)collagen gene (Col2a1) on eye structures in the 15-month-old C57BL/6JOlaHsd mouse was studied. The eyes were collected from C57BL mice heterozygous for a targeted inactivation of one allele of the Col2a1 gene (Col2a1(+/-) mice). The eyes of C57BL mice with normal gene alleles were used as controls (Col2a1(+/+) mice). Ocular histology was analyzed from tissue sections, stained with hematoxylin and eosin, toluidine blue and alcian blue. Type II collagen was localized by immunohistochemistry. Hyaluronan (HA) was stained utilizing the biotinylated complex of the hyaluronan-binding region of aggrecan and link protein (bHABC). The anterior segment of the eye was well-formed in both genotypes, but typical folding of ciliary processes was decreased, while increased stromal extracellular matrix vacuolization was seen in the Col2a1(+/-) mice. In the lens of these mice, subcapsular extracellular matrix changes were observed. Differences in retinal structures or the number of the eyes with retinal detachment were not detected between the genotypes. In Col2a1(+/-) mice, staining for type II collagen was weaker in cornea, ciliary body, iris, lens, vitreous, retina, choroid and sclera than in the control mice. HA staining was detected in the extraocular tissues, ciliary body, iris and the choroid of both genotypes. HA staining was observed only in the vitreous body of the control animals. Heterozygous inactivation of Col2a1 gene causes structural defects in the murine eye. The observed structural changes in the ciliary body, lens and vitreous of the Col2a1(+/-) mice may represent ocular features found in the human Stickler syndrome, where the abnormalities result from COL2A1 gene mutations which lead to functional haploinsufficiency.     

不同色素兔光化学法诱导视网膜静脉阻塞模型的对比

目的观察并比较光化学法诱导不同色素兔视网膜静脉阻塞（RVO）模型的各自特点与差异。方法普通级有色素兔和日本大耳白兔各10只。经兔耳缘静脉注入孟加拉红（40mg／kg）后,应用倍频532激光光凝兔双眼视网膜静脉主干,制作视网膜静脉阻塞模型。所有实验兔分别于术前和光凝后15min,1、3、7、14、21、28d行眼底彩照和荧光素眼底血管造影（FFA）检查,并于光凝后1d,2组各选取2只模型兔处死,摘除眼球行病理组织切片检查,观察比较不同色素兔眼底的损伤是否存在差异;其余于光凝后28d处死,摘除眼球行光学显微镜检查。结果2组实验兔光凝后均立刻出现视网膜血流阻断现象。光凝后1d,日本大耳白兔出现显著的视网膜水肿和少量视网膜下出血,普通有色素兔则表现为视网膜下火焰状出血和较为明显的视网膜水肿。2组FFA均显示视网膜两侧动静脉主干血流被阻断。2组实验兔在1～3周时,光凝点部位血管均出现不同程度的再通,视网膜出血水肿逐渐吸收。4周时血管基本再通,FFA示普通有色素兔光凝部位血管周围出现小范围的无灌注区、色素紊乱以及血管形态的异常。病理切片显示,光凝术后1d,日本大耳白兔脉络膜中可见血栓形成,而普通有色素兔则无此现象。2组实验兔均可观察到外层视网膜水肿。光凝后28d,2组实验兔均可观察到视网膜神经节细胞核密度减少。结论通过光化学诱导法,普通有色素兔及13本大耳白兔均可成功建立RVO模型。但不同色素兔使用相同激光能量制作RVO模型,眼底损伤部位存在差异。在眼底彩照和FFA检查上,2组有显著区别,且日本大耳白兔显影较差。     

Effects of lens extirpation with anterior vitrectomy on vitreous three-dimensional mesh structure

AIM: To investigate the changes in vitreous gel structure after lens extirpation combined with anterior vitrectomy in rabbit eyes. METHODS: Twenty-eight chinchilla rabbits were divided into three groups. The control group (Group I) included 16 eyes from eight rabbits who did not receive any treatment. Group II included 20 eyes from 10 rabbits that underwent lens aspiration only. Group III included 20 eyes from 10 rabbits that underwent lens aspiration combined with posterior capsulotomy and anterior vitrectomy. Eyes were harvested on the 30th and 60th day postoperatively, respectively. Changes in vitreous gel stretch length due to gravity and the rate of vitreous liquefaction were observed. The collagen content in the vitreous body was examined using the L-hydroxyproline test. Electronic microscopic images were obtained from each eyeball. RESULTS: On both the 30th and 60th day postoperatively, the vitreous gel length of group III was significantly shorter than group I and group II (P<0.05), while the rate of liquefaction of the vitreous body in group III was significantly higher than group I and group II (P<0.05). The collagen content in group III was also higher than that in group I and group II (P<0.05). CONCLUSION: Loss of vitreous gel mass is more likely to occur in the eyes of rabbits receiving anterior vitrectomy. Lensectomy combined with anterior vitrectomy may damage the stable three-dimensional mesh structure of collagen, which could aggravate vitreous gel liquefaction.