两种房水引流植入装置降眼压效果比较

目的 观察并比较两种房水引流装置植入术降眼压的效果。方法 选择健康新西兰白兔40只,单眼进行房水引流装置植入术。根据不同的植入物,分为NADI组和Ahmed组,每组20只实验兔。结果 术后各组均未出现浅前房。NADI组术后8周眼压比术前下降19.4%;Ahmed组术后8周眼压下降幅度为15.7%。术后8周内,各组间眼压值统计对比,均有显著性差异(P＜0.05),且NADI组的眼压值下降幅度要明显大于Ahmed组。结论NADI组比Ahmed组的眼压值下降幅度大,且下降时间维持较长,表明此新型房水引流植入物NADI降眼压效果明显,具有很好的临床应用前景。     

非穿透性小梁切除术联合羊膜植入治疗开角型青光眼

目的：评价非穿透性小梁切除术（non-penetrating trabecular surgery，NPIS）联合羊膜植入治疗开角型青光眼的临床疗效。方法：将23例（30只眼）具备手术适应证的开角型青光眼分为两组。Ⅰ组14例20眼，行NPIS联合羊膜植入术；Ⅱ组9例10眼，行NPIS手术联合透明质酸生物胶植入术。术后对两组患者的视力、眼压、滤过泡及并发症进行对比观察。结果：术后1个月时，Ⅰ组与Ⅱ组的视力变化比较，无显著差异（P〉0．05）；术后6、12、24月时，两组眼压值无显著差异（P〉0．05）。Ⅰ组术后早期有少量前房积血2只眼，轻度房水闪光5只眼；Ⅱ组术后早期1只眼有轻度房水闪光。结论：NPIS联合羊膜植入术与NPIS联合透明质酸生物胶植入术分别用于治疗开角型青光眼，其术后降眼压效果均较好（P〉0．05）。但前者的成本明显低于后者，可降低患者的经济负担。     

改良小梁切除术治疗青光眼的临床分析

目的 观察改良小粱切除术治疗青光眼的临床效果.方法 我院于2008年6月～2009年12月采用改良小梁切除术治疗青光眼患者132例(151眼),术中应用丝裂霉素C及可拆除缝线,术后随访1年,观察手术前后眼压、前房形成、滤过泡形态及并发症的情况.结果 手术后有85眼(56.29%)眼压控制于10～15mmhg,61眼(40.39%)眼压控制于16～21mmhg,4眼(2.64%)需配合降眼压滴眼液控制于10～21mmhg,1眼(0.66%)多次手术后植入房水引流阀门后眼压控制.术后第1天前房形成151眼(100%).出院时滤过泡均为扁平微隆,6个月后滤过泡形态稳定,观察至1年无改变:微小囊状型81眼,弥漫扁平型65眼,瘢痕型3眼,其中1眼最终植入房水引流阀,包裹型2眼.结论 改良小梁切除术在减少手术并发症的同时保证了手术的成功率,安全性高,临床疗效较好.     

超声乳化白内障吸除人工晶体植入治疗闭角型青光眼的临床优势分析

目的观察超声乳化白内障吸除人工晶体植入治疗闭角型青光眼的临床优势。方法选择2009年1月至2011年1月收住本院的闭角型青光眼64例（64眼）,根据入院顺序平分为两组-治疗组与对照组各32例。治疗组采用颞侧隧道式透明角膜切口超声乳化联合人工晶体植入术,对照组采用复合式小梁切除手术。结果两组术前视力相差不大,但是治疗后,治疗组术后最佳矫正视力大于0.8者8眼,0.3～0.8者20眼。治疗组的视力好转情况明显好于对照组（P〈0.05）。两组治疗前平均眼压比较无显著性差异（P〉0.05）,治疗后都有明显下降（P〈0.05）,治疗组的眼压下降幅度明显高于对照组（P〈0.05）。两组术中与术后并发症情况对比无显著性差异,具有可比性（P〉0.05）。结论超声乳化白内障吸除人工晶体植入治疗闭角型青光眼是一种可供选择的安全有效的手术方法,能有效提高视力与降低眼压,无术中与术后严重并发症发生,值得推广应用。     

难治性青光眼的Ahmed青光眼阀植入治疗:并发症与生物相容性

背景:近年来房水引流物的出现在治疗难治性青光眼上已经取得了较好的效果,但植入后会出现一些与材料有关的并发症,如炎症反应导致房水生成减少等原因引起低眼压及浅前房等。目的:观察Ahmed青光眼阀植入治疗难治性青光眼的效果及其生物相容性。方法:对32例(32眼)难治性青光眼实施Ahmed阀植入治疗,其中包括新生血管性青光眼12例,无晶状体眼青光眼6例,葡萄膜炎性青光眼4例,外伤性青光眼4例,有滤过手术失败史的青光眼6例,术后随访6～24个月。结果与结论:术前眼压4.655～9.044kPa,平均(5.61±1.29)kPa,末次随访时平均眼压(2.85±1.16)kPa,总有效率84.4%,其中新生血管性青光眼有效率83.3%,其他类型有效率85%。术后10眼视力较前有不同程度提高,最好视力达0.3。出现短暂性低眼压6例,浅前房6例,前房积血4例,内流管堵塞3例,经对症治疗后好转。结果表明Ahmed青光眼阀植入后降低眼压效果较好,但出现并发症比率较大,可能为引流装置设计和材料上的不足引起。     

经睫状体扁平部玻璃体切割术联合青光眼引流物植入治疗难治性青光眼

目的　旨在报告施行了经睫状体扁平部玻璃体切割术联合青光眼引流物植入患者的视力和眼压结果。方法　对 1990 .0 1.0 1～ 1998.0 2 .2 8日 Bascom Palm e眼科研究所施行了经睫状体扁平部玻璃体切割术联合青光眼引流物植入患者的医疗记录进行了回顾 ,全部患者均为本文作者所治疗者。40例患者 (4 0眼 )被确定 ,其中继发于增殖性糖尿病视网膜病变或视网膜中央静脉阻塞的新生血管性青光眼 14例 ,其他眼后节疾病 15例 ,继发性闭角性青光眼 7例 ,玻璃体前界膜破裂的无晶体眼 4例。测量的主要结果包括术后 1年的视力和眼压。结果　术后 1年 ,40例…     

联合手术治疗急性闭角型青光眼合并白内障的临床疗效

目的观察原发性急性闭角型青光眼(APACG)合并白内障两种手术方式的临床疗效及并发症。方法选择APACG合并白内障患者72例(96只眼),其中男性28例(38只眼),女性44例(58只眼)。将患者配对分为观察组和对照组,两组各36例(48只眼),观察组男性16例(24只眼),女性20例(24只眼),年龄49~75岁,平均年龄57.6岁;对照组男性12例(14只眼),女性24例(34只眼),年龄50~75岁,平均年龄58.5岁。观察组行超声乳化白内障吸除术并植入人工晶状体联合小梁切除术;对照组行超声乳化白内障吸除术并植入人工晶状体联合房角分离术。随访时间为4~18个月,随访期间,定期密切观察患者的视力、眼压、房角、前房深度及并发症等临床指标。结果对比眼压控制方面的术后疗效,观察患者在第1周、1个月、3个月、6个月、12个月随访发现,两组患者在术前和术后眼压降低幅度分别为(4.10±1.69)k Pa、(2.84±1.00)k Pa,差异具有统计学意义(t=2.168,P0.05)。中央前房深度加深幅度和房角形态变化及术后并发症,观察组和对照组术后中央前房深度加深幅度分别为(1.810 4±0.347 0)mm、(2.168 4±0.283 5)mm,差异有显著统计学意义(t=3.462,P0.01)。术后并发症,观察组术后虹膜纤维素样渗出及前房炎症、术后浅前房、角膜水肿的发生率分别比对照组高出8%、3%、2%,表明观察组术后并发症多于对照组。结论两种手术方式对APACG合并白内障患者的临床疗效安全有效;超声乳化白内障吸除术并植入人工晶状体联合小梁切除术在眼压控制更具有优势;在临床疗效方面,超声乳化白内障吸除术并植入人工晶状体联合房角分离术在中央前房深度加深幅度、房角形态变化和术后并发症控制更具有优势;观察组术后并发症多于对照组。     

血管抑素抑制兔眼表碱烧伤角膜缘移植术后的角膜血管新生

目的:检测眼表碱烧伤角膜缘移植术后血管抑素抑制角膜新生血管的作用。方法:16只新西兰大白兔双眼制作碱烧伤模型1d后,双眼行角膜缘移植术,术后左眼局部应用血管抑素治疗2周,右眼作对照;观测4周,根据新生血管侵入角膜缘内的范围、角膜混浊与水肿程度进行分级并作统计学处理;同时测量术后7、14、21及28d的眼压。结果:术后4周时,应用血管抑素的左眼的新生血管的评分为1.19±0.10,而对照组为1.63±0.72,统计学处理显示左眼的新生血管较右眼的明显减少(P<0.05),角膜混浊与水肿程度亦明显下降。各时间点各术眼的眼压均在正常范围,无统计学差异。结论:局部应用血管抑素能有效抑制眼表碱烧伤角膜缘移植术后的新生血管增生。     

小切口白内障囊外摘除人工晶状体植入术观察

目的观察小切口白内障囊外摘除人工晶状体植入术的临床效果：方法观察300例（396眼）小切口白内障囊外摘除人工晶体植入术的手术并发症及并发症的处理情况。结果术中并发症：后囊破裂16眼（4.04％），均一期植入后房型人工晶状体，无晶状体移位发生。术后并发症：角膜水肿56眼（14．14％），术后一周内药物治疗水肿消退。前房炎症反应26眼（6.57％），袁现为房水混浊、纤维素性渗出，药物治疗3-7天内消退，本组无角膜失代偿、视网膜脱离、人工晶状体脱位等严重并发症发生。结论小切口白内障囊外摘除术具有损伤小、恢复快、并发症少。适合基层医院开展等优点。     

复合式小梁切除术治疗青光眼的临床观察

目的评价复合式小粱切除术治疗青光眼的临床疗效。方法实施复合式小梁切除术治疗68例（74眼）各种类型青光眼，术中做以角膜缘为基底的结膜瓣，做4mm&#215;4mm以角膜缘为基底的约？巩膜厚度的板层巩膜瓣，术中使用抗代谢药物丝裂霉素C0．2mg／ml抑制溜过区瘢痕形成，前房穿刺，切除小梁组织2min&#215;2mm，虹膜根切，巩膜瓣顶端缝合2针，两侧边中央各缝合1针。结果随访半年，近期眼压控制良好，均在6mmHg～21mmHg之间。远期眼压：在6—21mmHg之间者为71眼（95．95％），术后均形成功能性滤过泡：Ⅰ型滤过泡19眼（25．68％）,Ⅱ型滤过泡55眼（74．32％）。Ⅰ度浅前房2只眼，Ⅱ度浅前房3只眼，无出现Ⅲ度浅前房，浅前房发生率676％。结论复合式小梁切除术可减少巩膜瓣，结膜下瘢痕形成，能主动调节房水滤过量，促进功能滤过泡形成，减少并发症的发生，提高手术的成功率。     

Intra-Scleral Ciliary Sulcus Suprachoroidal Microtube: Making Supraciliary Glaucoma Surgery Affordable

PurposeThe suprachoroidal space (SCS) has been a successful target to lower intraocular pressure (IOP) in glaucoma patients. We present the results of 4 patients who underwent a novel glaucoma surgical procedure to lower IOP: Intrascleral Ciliary Sulcus-Suprachoroidal Microtube.MethodsA sterile medical grade silicone microtube (Tube extender, New World Medical) was surgically placed to drain aqueous from the posterior chamber ciliary sulcus of the eye to the SCS. The internal diameter of the tube was 300 um and the length varied from 8-10mm. After informed consent was obtained and witnessed, this procedure was performed in glaucoma patients with pseudophakia. The tube was placed intrasclerally beneath an inferotemporal sclera flap (50% thickness approximately 4mm x 4mm). The anterior end of the tube was inserted into the ciliary sulcus approximately 2mm from the limbus and the posterior end was placed into the SCS approximately 4mm from the limbus. The microtube was sutured to the sclera with a 10-0 nylon suture. 8-0 vicryl sutures were used to close the sclera flap and the conjunctiva inferotemporally.ResultsAll 4 patients had lower IOP. The average reduction of IOP was 36% at 3 months. The amount of glaucoma medications per patient at 3 months dropped from an average of 3 to 0.25. The risks are similar to traditional glaucoma incisional surgery.ConclusionThis new technique of Intrascleral Ciliary Sulcus-Suprachoroidal Microtube in all four patients with mild, moderate, and advanced glaucoma demonstrated a significant lowering of IOP and a decrease in the number of medications. Further research is required to assess long term efficacy and safety.     

Identification of a fluorescein tracer model for determination of the flow rate of aqueous humor in the eye.

The continuous flow of the aqueous humor through the posterior and anterior chambers in the eye into Schlemm's canal is vital for the maintenance of a constant intraocular pressure. If the intraocular pressure rises above the normal range, several problems start appearing insidiously; for example, gradual visual field defects develop, leading ultimately to glaucoma. The determination of the flow rate of the aqueous humor is here performed by identifying a mathematical model after the free fluorescein concentration in the blood and in the anterior chamber of the eye has been measured. Experimental data obtained on rabbits are used in the analysis, and the flow rate of the aqueous humor in rabbit eyes is computed. This study demonstrates the feasibility of the approach in a clinical environment.     

一氧化氮在人工晶体植入术后眼内炎症反应中的作用

目的:探讨一氧化氮(NO)在人工晶体植入术后眼内炎症反应中的作用。方法:将新西兰白兔随机分成3组:(1)对照组;(2)L-精氨酸(L-Arg)组;(3)N-硝基-L-精氨酸(L-NNA)组。各组动物均施行晶体囊外摘除术(ECCE)+人工晶体囊袋内植入术(IOL),并于术后0、1、3、7、14、30 d观察术后眼内炎症反应,包括检查角膜水肿和前房渗出、房水细胞计数和分类;同时测定房水NO₂^-/NO₃^-含量。结果:L-Arg组前房渗出、房水细胞总数和NO₂^-/NO₃^-含量均高于对照组;而L-NNA组前房渗出、房水细胞总数和房水NO₂^-/NO₃^-含量均低于对照组。结论:NO在人体晶体植入术后眼内炎症反应中起一定的作用;使用NOS抑制剂可减少NO产生,降低术后眼内炎症反应。     

Effects of copper depletion andd-penicillamine treatment on the ocular inflammatory response

Rabbits placed on a copper (Cu)-deficient diet for four weeks had lower plasma Cu concentration, ferroxidase activity, and antioxidant activity than rabbits fed an identical Cu-adequate basel diet. Inflamed aqueous humor from rabbits on the Cu deficient diet also had less Cu, ferroxidase and antioxidant activity than inflamed aqueous humor from control rabbits. These differences mirrored antioxidant activity than inflamed aqueous humor from control rabbits. These differences mirrored changes in plasma levels. Furthermore, there was an increase in cellular infiltration into the aqueous humor of Cu-deficient rabbits. It is hypothesized that in Cu-deficient rabbits there is an increase in free radical production and formation of chemotactic substances in the eye due to the decreased aqueous humor concentration of the endogenous antioxidant, ceruloplasmin. It is therefore likely that ceruloplasmin plays a protective role in the intraocular inflammatory response.     

转化生长因子β1在兔房水中的浓度变化

背景：转化生长因子β1可参与角膜损伤后的修复。 目的：观察转化生长因子β1滴眼液滴眼后房水中的浓度变化规律。 方法：将新西兰大白兔随机分为5组,分别给予PBS和质量浓度为0.5,1.0,2.0,4.0 mg/L的转化生长因子β1滴眼液滴右眼。 结果与结论：通过裂隙灯观察兔角膜和结膜结构,各组兔眼均无结膜分泌物、球结膜充血、角膜水肿增厚、角膜后沉着物、前房炎性反应及晶状体混浊改变。ELISA检测结果显示,与PBS组比较,质量浓度2.0和4.0 mg/L转化生长因子β1滴眼液能有效提高兔眼房水中转化生长因子β1的质量浓度(P < 0.01),角膜穿透性良好,在房水中可以达到有效的治疗浓度。     

兔角膜碱烧伤模型房水中肿瘤坏死因子α及血管内皮生长因子表达与姜黄素的抑制

背景：稳定的角膜新生血管动物模型是研究角膜新生血管调控机制,姜黄素对碱烧伤角膜新生血管具有抑制作用和保护作用。 目的：探讨姜黄素对碱烧伤角膜新生血管模型中肿瘤坏死因子α及血管内皮生长因子表达的影响,为防治角膜新生血管提供理论依据。 方法：纳入33只新西兰大耳白兔,随机取3只设为正常组,其余30只建立兔角膜碱烧伤诱发角膜新生血管模型,右眼设为对照组给予生理盐水,左眼设为干预组给予姜黄素,裂隙灯观察角膜新生血管生长及角膜混浊情况,酶联免疫吸附实验检测肿瘤坏死因子α和血管内皮生长因子在房水中的表达。 结果：正常组没有角膜新生血管生成。与对照组比较,干预组角膜新生血管受到抑制且角膜混浊较轻(P < 0.05)。房水肿瘤坏死因子α和血管内皮生长因子在3组中均有表达,对照组和干预组明显高于正常组,但干预组低于对照组(P < 0.05)。说明姜黄素可以有效降低角膜碱烧伤后房水肿瘤坏死因子α及血管内皮生长因子的表达进而抑制兔角膜碱烧伤后角膜新生血管的生长。     

新型硅橡胶人工晶状体兔眼植入的生物相容性评价**

背景：软性人工晶状体的材料主要有硅凝胶、疏水性丙烯酸酯、亲水性丙烯酸酯和水凝胶等,但各材料优缺点不同,其长期生物学特性仍待临床检验。为改善白内障术后的视觉质量,提高人工晶状体的生物相容性及光学性能,进行新材料的开发是目前研究的热点。 目的：评价自主研制的新型硅橡胶后房型人工晶状体兔眼植入半年的生物相容性。 方法：选取20只新西兰白兔,均单眼行透明晶状体超声乳化吸除术联合人工晶状体植入,实验组(10眼)植入自主研制的硅橡胶(T-10)后房型人工晶状体,对照组(10眼)植入现已上市的硅凝胶后房型人工晶状体(EFC550)。 结果与结论：植入后早期,两组兔眼均有较重的前房渗出,差异无显著性意义。两组兔眼后囊膜混浊程度差异无显著性意义。植入后90 d及180 d,实验组虹膜后粘连情况轻于对照组。可见新型硅橡胶人工晶状体色素层生物相容性优于硅凝胶人工晶状体,具有临床可应用性。     

The relationship between cytokine level and nitric oxide content in aqueous humor after intraocular lens implantation

The relationship between cytokine level and nitric oxide content in aqueous humor after intraocular lens implantation     

From DNA damage to functional changes of the trabecular meshwork in aging and glaucoma

Glaucoma is a degenerative disease of the eye. Both the anterior and posterior segments of the eye are affected, extensive damage being detectable in the trabecular meshwork and the inner retina-central visual pathway complex. Oxidative stress is claimed to be mainly responsible for molecular damage in the anterior chamber. Indeed, oxidation harms the trabecular meshwork, leading eventually to endothelial cell decay, tissue malfunction, subclinical inflammation, changes in the extracellular matrix and cytoskeleton, altered motility, reduced outflow facility and (ultimately) increased IOP. Moreover, free radicals are involved in aging and can be produced in the brain (as well as in the eye) as a result of ischemia, leading to oxidation of the surrounding neurons. Glaucoma-related cell death occurs by means of apoptosis, and apoptosis is triggered by oxidative stress via (a) mitochondrial damage, (b) inflammation, (c) endothelial dysregulation and dysfunction, and (d) hypoxia. The proteomics of the aqueous humor is significantly altered in glaucoma as a result of oxidation-induced trabecular damage. Those proteins whose aqueous humor levels are increased in glaucoma are biomarkers of trabecular meshwork impairment. Their diffusion from the anterior to the posterior segment of the eye may be relevant in the cascade of events triggering apoptosis in the inner retinal layers, including the ganglion cells.     

Does the aqueous humor have a role in mitogen-activated protein kinase (MAPK) intracellular signaling in Glaucoma?

Glaucoma is a common blinding disease worldwide. Glaucoma treatment today is based on reduction of aqueous humor production or increase aqueous humor drainage. By medical manipulation, the treatment goal is to reduce the main risk factor, elevated intra ocular pressure. Here we hypothesize that the aqueous humor has a role, beside oxygen and nutrient supply, in transferring signaling to the trabecular meshwork. This signaling might be delivered from the ciliary body were the aqueous humor is produced, or from the lens or the cornea. Recently in our lab we proposed that MAPKs present in the aqueous humor are a novel signal involved in glaucoma pathology. Here we show that this pathway exists at an unexpected, extracellular media. Western blot analysis of aqueous humor from congenital glaucomatic rabbits and a rat model of induced elevated intra ocular pressure (IOP) were found to express several signaling members of the MAPK family. Although these members are usually found in an intracellular environment, they can be detected at an extracellular environment, namely the aqueous humor. These signaling proteins are found also in normal eyes. Moreover the MAPK signaling proteins are found in the active phosphorylated form and in non-active form in elevated IOP animals as well as in the control, normal IOP groups. Understanding the signaling cascade, at the aqueous humor, opens a new area for treatment of glaucoma patients. By interfering with the signaling cascade, taking place at a reachable location, the anterior chamber, we will be able to manipulate these protein effects on the trabecular meshwork.