骨髓间充质干细胞玻璃体腔移植对大鼠青光眼模型视神经的保护作用

目的：探讨骨髓间充质干细胞玻璃体腔移植对大鼠青光眼模型的神经保护作用。

方法：提取大鼠原代骨髓间充质干细胞并进行鉴定; Lewis大鼠分别随机分为3组：对照组、青光眼模型组和骨髓间充质干细胞组,并制作青光眼大鼠模型：左眼为实验眼(青光眼),右眼为对照眼,并进行鉴定; 然后进行骨髓间充质干细胞玻璃体腔移植; HE染色观察视网膜组织形态; 免疫荧光法检测视网膜神经节细胞数量; TUNEL染色观察视网膜神经节细胞凋亡情况; Western blot检测视网膜组织中IGF1和BDNF蛋白表达情况。

结果：大鼠实验眼的眼内压均明显高于对照眼(P<0.01),表明青光眼大鼠模型均建造成功; 青光眼模型组大鼠视网膜神经纤维排列不整齐,视网膜神经节细胞数量和视网膜厚度显著低于对照组(P<0.01),视网膜神经节细胞凋亡数量显著高于对照组(P<0.001); 骨髓间充质干细胞组大鼠视网膜神经纤维细胞排列较整齐,视网膜神经节细胞数量和视网膜厚度明显高于青光眼模型组(P<0.05),视网膜神经节细胞凋亡数量明显低于青光眼模型组(P<0.05); 青光眼模型组大鼠视网膜中IGF1和BDNF蛋白表达量明显低于对照组(P<0.01),骨髓间充质干细胞组大鼠的视网膜中IGF1和BDNF蛋白表达量高于青光眼模型组(P<0.05)。

结论：骨髓间充质干细胞玻璃体腔移植能改善大鼠青光眼,可以保护视网膜神经节细胞。     

两种方法治疗新生血管性青光眼的临床观察

目的：观察玻璃体腔内注射康柏西普联合小梁切除术或联合Ahmed青光眼引流阀植入术治疗新生血管性青光眼(NVG)的临床疗效。

方法：回顾分析2016-02/2017-06我院收治的NVG患者40例40眼,根据治疗方法分为A组(康柏西普联合小梁切除术+全视网膜光凝)和B组(康柏西普联合Ahmed青光眼引流阀植入术+全视网膜光凝),每组20例20眼。治疗后随访6mo,观察患者视力、眼压、眼压控制率和新生血管消退情况等。

结果：治疗前,两组患者眼压比较无差异(P>0.05)。治疗后6mo,B组眼压低于A组(P<0.05),但两组视力、眼压控制率、新生血管消退情况无差异(均P>0.05)。

结论：玻璃体腔注射康柏西普联合Ahmed青光眼引流阀植入和康柏西普联合小梁切除术治疗NVG安全有效,前者术式降眼压幅度更大。     

雷珠单抗联合小梁切除术治疗新生血管性青光眼

目的：探讨玻璃体腔内注射雷珠单抗联合小梁切除术治疗新生血管性青光眼(NVG)的疗效。

方法：收集2015-09/2017-04我院收治的NVG患者52例52眼的临床资料行回顾性分析,根据手术方式分为A组(玻璃体腔内注射雷珠单抗联合小梁切除术,31眼)和B组(玻璃体腔内注射雷珠单抗联合Ahmed青光眼阀植入术,21眼)。术后随访6mo,比较两组患者手术前后眼压和术后视力、视野、并发症情况,并评定临床疗效。

结果：两组患者术后眼压均逐渐降低,术后7d,1、3mo时A组患者眼压均低于B组(P<0.05)。术后6mo,两组患者视力和视野改变情况无明显差异(P>0.05),但A组患者治疗总有效率显著高于B组(97% vs 71%,P=0.013)。随访期间,A组患者角膜水肿、前房积血发生率均低于B组(均P<0.05)。

结论：玻璃体腔注射雷珠单抗联合小梁切除术治疗NVG,能有效降低并维持眼压水平,减少术后并发症,疗效显著。     

青光眼引流阀植入与小梁切除术治疗新生血管性青光眼的疗效比较

目的：探讨了玻璃体腔注射Bevacizumab联合引流阀植入术与小梁切除术治疗新生血管性青光眼的疗效和安全性。

方法：回顾性分析了我院2008-05/2010-05收治的22例23眼新生血管性青光眼患者的临床资料。所有患者均接受玻璃体腔注射Bevacizumab治疗,3～5d后根据患者接受治疗的方法分为青光眼引流阀植入术组(A组,13眼)和小梁切除术组(B组,10眼)。术后随访12～26mo,分别对两组术后视力、眼压、虹膜新生血管和并发症发生率进行比较。

结果：所有患者经Bevacizumab治疗3～5d后虹膜新生血管消退或大部分消退,有效率为100%。A组患者治疗后视力改善率明显高于B组(P<0.05),其中B组1例患者视力下降。A组和B组患者术后眼压较术前明显下降(P<0.05),而远期随访A组术后平均眼压明显低于B组(P<0.05)。A组和B组术后并发症发生率比较无统计学意义(P>0.05)。

结论：玻璃体腔注射Bevacizumab联合引流阀植入术治疗新生血管性青光眼可改善患者视力,较小梁切除术更有效控制眼压,且并发症少,值得临床推广使用。     

玻璃体腔注射Bevacizumab联合复合式小梁切除术治疗晚期新生血管性青光眼

目的：观察玻璃体腔注射bevacizumab联合复合式小梁切除术治疗新生血管性青光眼的临床疗效。

方法：选取2011-02/2013-09间在我院接受治疗的46例晚期NVG患者。分为两组,每组23例,A组为观察组,行玻璃体腔注射bevacizumab联合复合式小梁切除术,B组为对照组,给睫状体冷凝术治疗。术后对两组患者视力、眼压、虹膜新生血管、术后并发症进行对比观察,随访12mo。

结果：两组术后眼压均较术前下降,A组术后眼压水平低于B组,差异有统计学意义(P<0. 05),A组治疗成功19例(83%), B组治疗成功12例(52%),差异有统计学意义(χ²=4.847,P=0.028)。

结论：玻璃体腔注射bevacizumab联合复合式小梁切除术治疗NVG能够有效控制眼压,成功率较高。     

康柏西普玻璃体腔注射联合EX-PRESS青光眼引流器植入治疗NVG

目的：观察康柏西普玻璃体腔注射应用EX-PRESS青光眼引流器植入治疗新生血管性青光眼的疗效。

方法：选择2015-01/2018-01在我院眼科就诊的新生血管性青光眼患者37例37眼,随机分为试验组与对照组,两组在术前均行康柏西普玻璃体腔注射,试验组和对照组分别选择EX-PRESS青光眼引流器植入术和小梁切除术。对比两组术后成功率、最佳矫正视力、眼压、滤过泡、并发症。

结果：术后12mo, 两组手术成功率、BCVA及滤过泡率均无差异(P>0.05)。两组不同时间点眼压比较有差异(F_组间=10.0,P_组间=0.003; F_时间=496.27,P_时间<0.0001)。所有并发症经对症处理后改善。

结论：EX-PRESS青光眼引流器植入联合康柏西普玻璃体腔注射治疗新生血管性青光眼对降低眼压、减少术后并发症有一定的临床价值。     

玻璃体腔注射TA对光化学诱导大鼠BRVO模型血管生成及Notch通路的影响

目的：探讨玻璃体腔注射曲安奈德(TA)对光化学诱导大鼠视网膜分支静脉阻塞(BRVO)模型血管生成及Notch通路的影响。

方法：制备光化学诱导BRVO大鼠模型,随机分为BRVO模型组、玻璃体腔注射TA后1、7、21d组; 同时设置空白对照组进行对照。眼压计测量大鼠眼压状况; 眼底彩照、荧光素眼底血管造影(FFA)和光学相干断层扫描(OCT)观察大鼠眼底情况; 蛋白免疫印迹法(WB)检测大鼠视网膜血管生成相关因子血管内皮细胞生长因子(VEGF)、血管内皮生长因子受体2(VEGFR2),Notch通路重要因子Notch1、Jagged1、DLL4蛋白表达情况。

结果：正常对照组眼底血管排列整齐、状态清晰。BRVO模型组眼底出现水肿,视网膜变白,血管排列紊乱,视盘凹消失,视网膜血管收缩。玻璃体腔注射TA后1、7、21d组水肿逐渐减轻,血管扩张和弯曲逐渐减缓,视盘凹恢复。与空白对照组相比,BRVO模型组眼压升高,损伤处视网膜、损伤250μm处视网膜厚度增加,VEGF、VEGFR2、Notch1、Jagged1蛋白表达升高,DLL4蛋白表达降低(P<0.05)。与BRVO模型组相比,玻璃体腔注射TA后 1d组损伤250μm处视网膜厚度减少,VEGFR2、Notch1、Jagged1蛋白表达降低,DLL4蛋白表达升高; 玻璃体腔注射TA后7d组损伤处视网膜、损伤250μm处视网膜厚度减少,VEGFR2、Notch1、Jagged1蛋白表达降低,DLL4蛋白表达升高; 玻璃体腔注射TA后21d组眼压降低,损伤处视网膜、损伤250 μm处视网膜厚度减少,VEGF、VEGFR2、Notch1、Jagged1蛋白表达降低,DLL4蛋白表达升高(P<0.05)。

结论：玻璃体腔注射TA可能通过调控Notch通路抑制VEGF激活从而抑制血管生成,实现对BRVO大鼠视网膜保护作用。     

非缺血型视网膜分支静脉阻塞黄斑水肿抗VEGF治疗的疗效研究

目的：探究雷珠单抗与康柏西普治疗非缺血型视网膜分支静脉阻塞黄斑水肿的疗效及安全性。

方法：选取我院于2014-03/2018-05收治的非缺血型视网膜分支静脉阻塞黄斑水肿患者80例80眼,随机分为A组(40例)和B组(40例),分别行玻璃体腔内注射雷珠单抗和康柏西普治疗。随访3mo,比较治疗前后两组患者的眼压、CMT、黄斑中心体积(CMV)、BCVA、玻璃体腔注射次数和并发症发生情况。

结果：治疗后2wk,1、2、3mo,B组患者CMT、CMV、BCVA均明显优于A组(P<0.05)。随访3mo,B组患者视力提高比例显著高于A组(65% vs 38%,P<0.05),玻璃体腔注射次数显著低于A组(P<0.05),但两组患者并发症发生情况(5% vs 0%)无明显差异(P=0.999)。

结论：与雷珠单抗比较,康柏西普治疗非缺血型视网膜分支静脉阻塞黄斑水肿在改善视力,降低CMT和CMV,减少玻璃体腔注射次数方面具有一定优势。     

雷珠单抗辅助玻璃体切割和PRP联合小梁切除术治疗NVG的疗效

目的：观察雷珠单抗辅助玻璃体切割+全视网膜光凝(PRP)+小梁切除术治疗新生血管性青光眼(NVG)的临床疗效。

方法：回顾性分析2017-03/2018-10收治的NVG患者44例44眼,采用玻璃体腔内注射雷珠单抗+玻璃体切割+PRP+小梁切除手术治疗的患者22例22眼(A组),采用玻璃体腔内注射雷珠单抗+小梁切除+PRP治疗的患者22例22眼(B组)。术后随访6mo,观察患者视力、眼压、眼压控制率、新生血管及并发症等情况。

结果：治疗前两组患者眼压无差异(46.2±9.41mmHg vs 49.1±10.15mmHg,P>0.05),治疗后1wk,1、6mo A组患者眼压均低于B组(P<0.05)。治疗后6mo,A组视力、眼压控制率(95%)、新生血管消退情况(91%)均优于B组(P<0.05),但随访期间两组患者并发症发生率无差异(P>0.05)。

结论：雷珠单抗辅助玻璃体切割+PRP+小梁切除术治疗NVG安全有效,可稳定持久地控制眼压,改善部分患者视力。     

康柏西普联合PRP治疗视网膜中央静脉阻塞继发早期新生血管性青光眼

目的：对比研究玻璃体腔注射康柏西普联合全视网膜激光光凝(PRP)与单纯全视网膜激光光凝对视网膜中央静脉阻塞(CRVO)继发Ⅰ、Ⅱ期新生血管性青光眼治疗效果的临床观察。

方法：采取临床病例对照研究方法。将2014-01/2019-03在我院诊断为CRVO继发Ⅰ、Ⅱ期新生血管性青光眼患者60例60眼,随机分为联合治疗组和单纯治疗组。联合治疗组采用康柏西普联合全视网膜激光光凝治疗; 单纯治疗组采用单纯全视网膜激光光凝治疗。观察两组患者治疗前、治疗后1wk,1、3、6、9mo的视力、眼压、虹膜新生血管、房角新生血管的情况,进行统计学分析。

结果：不同时间点两组房角及虹膜新生血管数量和视力、眼压有差异(F=154.992、92.519、30.696、82.374,均P<0.001),联合治疗组在治疗开始后1wk的各项指标均出现明显好转,并维持至治疗结束。而单纯治疗组在给予治疗后数据改善程度不及联合治疗组(F=50.870、24.265、13.125、11.829,均P<0.001)。

结论：玻璃体腔注射康柏西普联合全视网膜激光光凝治疗CRVO继发Ⅰ、Ⅱ期新生血管性青光眼疗效优于单纯全视网膜激光光凝治疗,效果显著并持续维持。     

Obstructed axonal transport of BDNF and its receptor TrkB in experimental glaucoma

PURPOSE: In both animal model system and in human glaucoma, retinal ganglion cells (RGCs) die by apoptosis. To understand how RGC apoptosis is initiated in these systems, the authors studied RGC neurotrophin transport in experimental glaucoma using acute intraocular pressure (IOP) elevations in rats and chronic IOP elevation and unilateral optic nerve transections in monkeys. METHODS: Eyes were studied in masked fashion by light and electron microscopy and by immunohistochemistry with antibodies directed against the tyrosine kinase receptors (TrkA, B, and C) and against brain-derived neurotrophic factor (BDNF), as well as by autoradiography to identify retrograde axonal transport of 125I-BDNF injected into the superior colliculus. RESULTS: With acute glaucoma in the rat, RGC axons became abnormally dilated, accumulating vesicles presumed to be moving in axonal transport at the optic nerve head. Label for TrkB, but not TrkA, was relatively increased at and behind the optic nerve head with IOP elevation. Abnormal, focal labeling for TrkB and BDNF was identified in axons of monkey optic nerve heads with chronic glaucoma. With acute IOP elevation in rats, radiolabeled BDNF arrived at cells in the RGC layer at less than half the level of control eyes. CONCLUSIONS: Interruption of BDNF retrograde transport and accumulation of TrkB at the optic nerve head in acute and chronic glaucoma models suggest a role for neurotrophin deprivation in the pathogenesis of RGC death in glaucoma.     

Measurement of amino acid levels in the vitreous humor of rats after chronic intraocular pressure elevation or optic nerve transection

PURPOSE: To investigate whether the levels of free amino acids and protein in the vitreous of rat eyes are altered with chronic intraocular pressure (IOP) elevation or after optic nerve transection. MATERIALS AND METHODS: The concentrations of 20 amino acids in the vitreous humor were measured by high-performance liquid chromatography in both eyes of 41 rats with unilateral IOP elevation induced by translimbal photocoagulation. Eyes were studied 1 day and 1, 2, 4, and 9 weeks after initial IOP elevation. The same amino acids were measured in 41 rats 1 day and 2, 4, and 9 weeks after unilateral transection of the orbital optic nerve. The intravitreal protein level was assayed in additional 22 rats with IOP elevation and 12 rats after nerve transection. Two masked observers evaluated the amount of optic nerve damage with a semiquantitative, light-microscopic technique. RESULTS: In rats with experimental glaucoma, amino acid concentrations were unchanged 1 day after treatment. At 1 week, 4 of 20 amino acids (aspartate, proline, alanine, and lysine) were higher than in control eyes ( < or = 0.01), but this difference was nonsignificant after Bonferroni correction for multiple simultaneous amino acid comparisons (none achieved < 0.0025). No amino acid was significantly different from control in the nerve transection groups (all > 0.05). Vitreous protein level was significantly higher in glaucomatous eyes than their paired controls at 1 day ( < 0.0001) and 1 week ( < 0.002). One day and 1 week after optic nerve transection, vitreal proteins were significantly elevated compared with control eyes from untreated animals ( < 0.0020 and < 0.0022, respectively), though not compared with their fellow eyes ( = 0.25 and 0.10). CONCLUSION: Chronic experimental glaucoma and transection of the optic nerve increase the amount of protein in the rat vitreous above control levels. In the vitreous of rats with experimental glaucoma, a number of free amino acids were transiently elevated to a modest degree, but no significant difference in vitreous glutamate concentration was detected ( > 0.01).     

A submicron emulsion of HU-211, a synthetic cannabinoid, reduces intraocular pressure in rabbits

Purpose: To study the ocular hypotensive effect of a nonpsychotropic cannabinoid, HU-211 (11-hydroxy-Δ⁸-tetra-hydrocannabinol, dimethylheptyl), an N-methyl-D-aspartate (NMDA) agonist, in normotensive rabbits. Methods: The cannabinoid HU-211, being lipophilic, was incorporated into a stable oil-in-water submicron sterile emulsion, consisting of 0.12% (w/w) HU-211. A single- dose, randomized and double-masked study was designed, using a Digilab 30R pneumotonometer to measure intraocular pressure (IOP) in normotensive rabbits. Results: Application of a single dose of HU-211 ophthalmic preparation resulted in an IOP reduction of 5.3 mmHg (24% of baseline), first evident at 1.5 h post application and persisting for over 6 h. A small but significant lowering of pressure (12.5% of baseline) occurred in the contralateral eyes of HU-211 treated rabbits, lasting for 4 h post treatment. Conclusion: Our work demonstrated that HU-211, incorporated into submicron emulsion, caused a 6-h-long reduction in IOP in the treated eye, with a lesser reduction in the contralateral untreated eye. Received: 30 March 1999 Revised: 10 June 1999 Accepted: 10 June 1999     

超声微泡造影剂介导脑源性神经营养因子联合转染视网膜和视皮质对视神经损伤后视网膜神经节细胞的保护作用

　　目的　观察超声微泡造影剂介导脑源性神经营养因子（BDNF）联合转染大鼠视网膜和视皮质区细胞对视神经损伤后视网膜神经节细胞（RGC）的保护作用。方法　雄性Sprague-Dawley（SD）大鼠88只随机分为正常组（A组）、假手术组（B组）、空白对照组（C组）、单纯眼转染组（D组）、单纯脑转染组（E组）、联合转染组（F组）;A组8只大鼠,B～F组每组16只大鼠。建立钳夹视神经损伤模型,将B～F组大鼠随机分为视神经损伤1、2周亚组,各亚组8只大鼠。B、C组玻璃体腔和视皮质区分别注射磷酸盐缓冲液（PBS）,D、E组玻璃体腔和视皮质区分别注射BDNF质粒（pBDNF）微泡造影剂悬液,F组玻璃体腔和视皮质区同时注射pBDNF微泡造影剂悬液。D～F组注射pBDNF微泡微泡造影剂悬液后,立即用超声辐照相应转染部位。视神经损伤后1、2周,各组行逆行荧光金标记RGC计数;半胱氨酸蛋白酶-3(caspase-3）蛋白免疫组织化学染色,观察其阳性表达情况;图形视网膜电流图（PERG）检测,记录N95振幅。结果　荧光金标记RGC结果显示,各组均可见金黄色荧光散布于视网膜定向铺片上。A~F组间RGC计数差异有统计学意义（F=256.30,P＜0.01）;B~F组视神经损伤1、2周亚组间RGC计数差异也有统计学意义（F=6518,P＜0.01）。光学显微镜观察发现,A、B组大鼠视网膜均未见caspase-3蛋白阳性表达;C~F组均可见主要位于神经节细胞层的caspase-3蛋白阳性表达。PERG检测发现,A~F组间N₉₅振幅差异有统计学意义（F=121.56,P＜0.01）;B~F组视神经损伤1、2周亚组间N95振幅差异也有统计学意义（F=8238,P＜0.01）。结论　超声微泡造影剂介导BDNF联合转染视网膜和视皮质区细胞能抑制视神经损伤后RGC凋亡,提高RGC存活数,保护其视功能。      

睫状神经营养因子玻璃体内注射对青光眼视神经保护作用的实验研究

目的探讨睫状神经营养因子（CNTF）玻璃体内注射对鼠慢性青光眼视神经的保护作用。方法通过散瞳、前房穿刺放液及角膜缘激光光凝等步骤制造鼠慢性青光眼模型。设正常对照组、前房穿刺对照组、未治疗组（仅造模）、治疗组（造模后双眼玻璃体内注入CNTF）、治疗对照组（造模后双眼玻璃体内注入生理盐水）。观察视网膜组织磷酸化信号转导与转录激活子3（pSTAT3）表达、视神经轴突及闪光视觉诱发电位（F-VEP）变化。结果正常状态pSTA33在视网膜组织中极少表达,眼压升高后1d开始上升,2d达到高峰,14d下降到正常水平。治疗组视网膜中pSTAT3在眼压升高14d和28d表达均高于同时间段的未治疗组及治疗对照组（P〈0．05）。在眼压升高28d治疗组视神经纤维阳性面积比率的值明显高于未治疗组及治疗对照组,且VEPP,波潜伏期明显低于以上两组（P〈0．05）。结论CNTF玻璃体内注射延缓了鼠慢性青光眼视神经的损伤。眼压升高初期,视网膜STAT3信号传导途径暂时被激活,CNTF相对长时间激活了STAT3信号传导途径,STAT3信号传导途径参与介导了CNTF对视神经的保护作用。     

Selective ganglion cell functional loss in rats with experimental glaucoma

PURPOSE: To characterize retinal functional consequences of elevated intraocular pressure (IOP) in a rat model of experimental glaucoma. METHODS: Unilateral elevation of IOP was produced by hypertonic saline injection into an episcleral vein in 20 adult male Brown-Norway rats. IOP was measured in both eyes of awake animals four to five times per week. After 5 weeks, animals were dark adapted overnight (>12 hours) and full-field electroretinograms (ERGs) were obtained simultaneously from both eyes. Scotopic ERG stimuli were brief white flashes (-6.64-2.72 log cd-s/m(2)). Photopic responses were also obtained (0.97-2.72 log cd-s/m(2)) after 15 minutes of light adaptation (150 cd/m(2)). Eyes were processed the following day for histologic evaluation by light microscopy, including masked determination of optic nerve injury grade (ONIG; 1, normal; 5, severe, diffuse damage). RESULTS: Among experimental eyes, the group average IOP (+/-SD) was 34.5 +/- 4.1 mm Hg, whereas the average for control eyes was 28.1 +/- 0.5 mm Hg (t = 7.1, P < 0.0001). The average ONIG for experimental and control eye groups, respectively, was 3.4 +/- 1.7 and 1.0 +/- 0.02 (t = 6.3, P < 0.0001). The ONIG increased with mean IOP in experimental eyes (r(2) = 0.78, P < 0.0001) and was unrelated to mean IOP in control eyes (r(2) = 0.09, P = 0.18). In experimental eyes with relatively mild IOP elevation (mean IOP < 31 mm Hg) and no structural (histologic) damage to the optic nerve evident by light microscopy (ONIG = 1.1 +/- 0.2, n = 5), there was a selective reduction of the positive scotopic threshold response (pSTR; P < 0.001), whereas other ERG components remained unaltered. In four of the five eyes, pSTR amplitude was reduced by more than 50%, whereas all five had normal scotopic a-wave, b-wave, and OP amplitudes. Eyes with mean IOP of more than 35 mm Hg had reduced a-wave, b-wave, and oscillatory potential (OP) amplitudes. CONCLUSIONS: As demonstrated by prior studies, selective loss of the pSTR is indicative of selective retinal ganglion cell (RGC) injury. In this rat model of experimental glaucoma, selective RGC functional injury occurred before the onset of structural damage, as assessed by light microscopy of optic nerve tissue. The highest IOP levels resulted in nonselective functional loss. Thus, in rodent models of experimental glaucoma, lower levels of chronically elevated IOP may be more relevant to human primary chronic glaucoma.     

Ahmed引流阀植入联合玻璃体腔注射Bevacizumab治疗NVG

目的：观察Ahmed引流阀植入联合玻璃体腔注射bevacizumab(贝伐珠单抗)治疗新生血管性青光眼(neovascular glaucoma,NVG)的疗效。

方法：对22例22眼新生血管性青光眼患者先进行玻璃体腔注射bevacizumab 0.1mL(2.5mg),待虹膜新生血管消退后行Ahmed青光眼阀门植入术。术后观察视力、眼压、虹膜新生血管消退情况、术中及术后并发症,随访6～36(平均24)mo。

结果：玻璃体腔注药后1wk内22眼虹膜新生血管均有不同程度消退,Ahmed引流阀植入术后随访22眼中仅有3眼联合使用1～3种抗青光眼药物,眼压控制在21mmHg之内,1眼因眼压失控而行睫状体光凝术(810激光),其余18眼均无需加用抗青光眼药物眼压控制在正常范围内,最后一次随访,平均眼压15.59±3.21mmHg,与术前平均眼压(45.36±8.13mmHg)相比,差异有统计学意义(P<0.05)。视力提高者9眼(41%),保持术前视力者13眼。全部病例在玻璃体腔注射bevacizumab及Ahmed引流阀植入术中术后均未观察到严重手术并发症。

结论：Ahmed引流阀植入联合玻璃体腔注射bevacizumab治疗NVG安全有效,手术成功率高,并发症少,有利于保护残留视功能。     

Neuroprotective effect of systemic and/or intravitreal rosuvastatin administration in rat glaucoma model

AIM: To evaluate the neuroprotective effect of rosuvastatin, in a rat experimental glaucoma model. METHODS: Ocular hypertension was induced in right eyes of Long-Evans rats (n=30) by cauterization of three episcleral veins. Left eyes were defined as controls. Rats were divided into five groups: oral rosuvastatin, intravitreal rosuvastatin, oral+intravitreal rosuvastatin, intravitreal sham and glaucoma without intervention. Rats were sacrificed at day 14. Retinal ganglion cell (RGC) number was assessed by histopathological analysis. Terminal deoxynucleotidyl transferase-mediated dUTP-nick end-labeling (TUNEL) staining and the expression of glial fibrillary acidic protein (GFAP) in RGC layer was also examined. RESULTS: A significant intraocular pressure (IOP) elevation was seen (P=0.002). Elevated IOP resulted in a significant decrease in number of RGCs in group 5 (70.33±8.2 cells/mm²) when compared with controls (92.50±13.72 cells/mm²; P=0.03). The RGC number in group 1 (92.4±7.3 cells/mm²) was significantly higher than group 5 (P=0.03). The numbers of RGC in groups 2, 3 (57.3±8.2 cells/mm², 60.5±12.9 cells/mm²) were comparable with that of group 5 (P=0.18 and P=0.31). The apoptosis rates with TUNEL staining were also parallel to RGC number. Animals with experimentally induced glaucoma showed an increase in retinal GFAP immunoreactivity. CONCLUSION: Decrease in RGC loss and apoptosis suggest the neuroprotective potential of oral rosuvastatin treatment in a rat model of ocular hypertension. However intravitreal rosuvastatin showed a contrary effect and further studies are required.     

新生血管性青光眼患者药物联合小梁切除术的安全性分析

目的：观察抗血管内皮生长因子( vascular endothelial growth factor,VEGF)药物联合小梁切除术治疗新生血管性青光眼患者后其视力及眼压变化,以探究此联合治疗方法的有效性和安全性。
　　方法：将2012-08/2014-08在我院眼科定期复查且随访时间>6 lo的60例60眼青光眼患者采用随机数字法均分为A组(观察组)和B组(对照组),观察组给予玻璃体腔注射雷珠单抗联合小梁切除术治疗;对照组予以睫状体冷凝术治疗。术后观察患者视力变化、眼压、虹膜及房角新生血管等。
　　结果：视力：术后A组视力提高9眼显著高于B组,视力下降5眼显著低于B组,差异有统计学意义(P<0.05)。眼压：A组术眼玻璃体腔注射雷珠单抗后眼压无明显下降,行小梁切除术后眼压明显下降并能基本保持平稳,术后1wk A组14.6±3.7llHg显著低于B组;B组患者治疗后眼压逐渐下降,手术1 lo以后基本稳定。 A组术后1、3、6 lo眼压水平分别显著低于B组,差异有统计学意义(P<0.05),末次随访12lo 末,A 组治疗成功26眼(87%),有4眼眼压>30llHg,但患者症状减轻,显著高于B组治疗成功14眼(47%),13眼眼压>30llHg,症状减轻,3眼眼压<7llHg,眼球未萎缩,两组治疗成功率比较差异有统计学意义(P=0.026)。 A 组并发症发生率(13%)显著低于B组(67%),差异有统计学意义(P<0.05)。
　　结论：抗VEGF药物联合小梁切除术治疗新生血管性青光眼可提高患者视力、降低眼压、缓解症状,安全性较好。