5-氟尿嘧啶联合低分子肝素兔前房灌注的毒性研究

目的观察5-氟尿嘧啶和低分子肝素的联合使用对兔眼组织所产生的不良作用,为其在临床上的使用奠定安全基础。方法健康纯种新西兰白兔14只,取左眼为A组,右眼为B组。将低分子肝素和5-氟尿嘧啶注入到BSS中,配成浓度为低分子肝素5×103IU·L-1,5-氟尿嘧啶0.25g·L-1的灌注液。A组药物前房灌注时间为30min,B组药物前房灌注时间为60min。术后1d、4d、7d均行裂隙灯检查,Schiotz眼压计检测双眼眼压,并行角膜内皮照相及组织学检查。结果2组术后炎症反应轻微,角膜保持透明。前房内未见有明显的纤维素性渗出和出血,眼压和角膜内皮计数检查术前与术后没有差异。光镜下2组角膜组织5层结构清晰,上皮细胞排列整齐,前弹力层完整,基质层纤维排列规则,后弹力层均匀,内皮细胞单层扁平上皮连续,形态规整。结论兔眼对浓度为5×103IU·L-1的低分子肝素、0.25g·L-1的5-氟尿嘧啶的灌注液有较好的耐受性。     

氟尿嘧啶联合低分子肝素预防增殖性玻璃体视网膜病变的视网膜电图

目的:利用视网膜电流图探讨氟尿嘧啶及低分子肝素联合用药,预防玻璃体切除术后增殖性玻璃体视网膜病变发生过程中的安全性。方法:随机选择有发生增殖性玻璃体视网膜病变高风险视网膜脱离患者132例132眼,分为干预组和对照组各66眼。干预组术中灌注液中加入氟尿嘧啶及低分子肝素灌注60min。对照组术中灌注液不用任何药物;所有患者术前、术后3,6mo检查视网膜电流图,用配对t检验比较两组各期视网膜电流图有无差异。结果:干预组术后PVR发生率显著低于对照组;两组间各期视杆细胞反应a波、b波;最大反应a波、b波;明视反应a波、b波幅值和潜峰时和∑Ops幅值无显著差异。两组间各期视力无显著差异。结论:氟尿嘧啶及低分子肝素联合用药可以预防增殖性玻璃体视网膜病变发生,且对视网膜视杆细胞、视锥细胞、视网膜微循环功能无严重影响。     

氟尿嘧啶脂质体玻璃体内注射对兔视网膜毒性

目的了解氟尿嘧啶脂质体玻璃体内注射对兔眼视网膜的毒性作用,探索其安全剂量范围。方法30只家兔,随机分为5组。右眼为实验眼,玻璃体内注射药物,其中氟尿嘧啶脂质体组,浓度分别为0.8 mg/0.1 mL,1.6 mg/0.1 mL,3.2 mg/0.1 mL,6.0 mg/0.1 mL;游离氟尿嘧啶组,浓度为1.6 mg/0.1 mL。左眼为对照眼,注射磷酸缓冲液0.1 mL。注药前后分别行双眼闪光及图形视网膜电图检查,求出双眼振幅平均值的比率(实验眼/对照眼)。注药后第28天摘除眼球行光镜和透射电镜检查。结果氟尿嘧啶脂质体组浓度0.8 mg,1.6 mg,3.2 mg剂量组未见视网膜电图及光镜下异常.6.0 mg氟尿嘧啶脂质体组及1.6 mg游离氟尿嘧啶组均呈现视网膜电图及光镜下异常。透射电镜在3.2 mg剂量脂质体组即发现视网膜结构异常。结论脂质体作为氟尿嘧啶的缓释载体能降低其视网膜毒性作用,其玻璃体内注射的最大安全剂量不超过1.6 mg。     

玻璃体切除术中气体灌注对兔眼视网膜的损伤

目的探讨玻璃体切除术中气体灌注对兔眼视网膜形态结构及生理功能的影响,以期明确玻璃体切除术后视功能受损的机制。方法将24只灰兔随机分成3组行玻璃体切除术,A、B两组分别在25和40mmHg(1mmHg=0．133kpa)的气体灌注压下行气液交换,对照组不做气液交换。术后行临床观察及视网膜电图检查,6周后摘除眼球行光镜及透射电镜检查。结果临床观察各组兔眼未见明显异常体征。术后1d,A、B两组视网膜电图bA比值与对照组相比差异均有显著意义,术后6周B组bA比值仍显著降低。光镜下可见B组兔眼灌注后对侧视网膜结构紊乱伴部分组织缺失,视网膜厚度与对照组相比有明显差异,其中外层视网膜厚度降低更加明显。电镜下可见B组兔眼灌注后对侧视网膜有较明显的神经纤维及光感受器细胞损伤,A组兔眼损伤表现轻微。各组兔眼灌注侧视网膜未见异常。结论玻璃体切除术中气体灌注可造成兔眼视网膜的不可逆损伤,气体灌注可能是玻璃体切除术后视功能受损的主要原因之一。（中华眼科杂志,2004,40：760—764)     

氟尿嘧啶联合低分子肝素防治增殖性玻璃体视网膜病变的临床观察

目的评价氟尿嘧啶联合低分子肝素在预防玻璃体切割术后增殖性玻璃体视网膜病变发生过程中的安全性和有效性。方法本研究随机选择本科2003．4～2003．11间需行玻璃体手术治疗的视网膜脱离患者50例50眼，病例选用标准为具有玻璃体术后视网膜脱离复发的高危因素的患者，分成治疗组与对照组，治疗组灌注液中加入低分子肝素和氟尿嘧啶，药物灌注时间控制在35～45分钟之间，随访3个月，对两组结果进行对比分析结果随访3个门后，治疗组与对照组术后增殖性玻璃体视网膜病变的发生率分别为8％(2／25)和36%(9/25)，有显著性差异(P=0．041),治疗组术后因PVR造成的视网膜脱离复发率为4％(1／25)，对照组为16%(4／25)，治疗组1例和对照组4例患者成功的进行了视网膜的再次复位手术。没有发现有明显的与药物有关的眼部并发症。结论虽然术后3个月时两组视网膜脱离的复发率差异没有统计学意义，但治疗组术后增殖性玻璃体视网膜病变的发生率较对照组有意义的减少。本试验显示了手术联合氟尿嘧啶与低分子肝素可以预防术后PVR的发生。     

曲安奈德对兔视网膜组织和细胞形态学影响的实验研究

目的 观察玻璃体内注射去除溶媒后的两种商用曲安奈德（TA）对兔眼视网膜结构的影响及其与剂量的关系。设计 实验研究。研究对象 新西兰白兔21只。方法 将实验动物分为A（药物A）、B（药物B）、C（平衡盐溶液）三组,A组分为A1、A2、A3三个亚组,B组分为 B1、B2两个亚组,C组分为C1、C2两个亚组。用梯度离心法去除两种商用TA注射液（药物A、药物B）中的溶媒,获取TA颗粒。向A1、A2和A3组兔右眼玻璃体内分别注入4 mg、20 mg和40 mg药物A;向B1、B2组兔右眼玻璃体内分别注入4 mg和20 mg的药物B;向C1和C2组兔右眼玻璃体内分别注入0.1 ml和0.2 ml平衡盐溶液作为对照。注药前、后行眼前段及眼底检查。术后8周眼球摘除在光镜下行视网膜组织学检查及用透射电镜观察视网膜细胞结构。主要指标 眼底形态、视网膜光镜结构、光感受器细胞电镜结构。结果 注射后8周所有注射眼均未出现眼前段及眼底异常。光镜检查显示：与未注射眼相比,C组及A组兔眼视网膜结构大致正常,B组兔眼光镜下出现内层、外层视网膜结构紊乱,B2组较B1组更为明显;透射电镜检查显示：与未注射眼比较,C1、C2组兔眼部分线粒体出现水肿、嵴断裂,C1组较C2组更为明显,膜盘形态及光感受器细胞核形态大致正常;A1、A2、A3组兔眼可见轻度光感受器膜盘水肿,而细胞核、线粒体结构无明显改变,且线粒体嵴随注射剂量增加排列更为整齐;B1、B2与未注射眼、C组以及A组相比,光感受器膜盘明显水肿,细胞核皱缩和广泛线粒体水肿、嵴断裂缺失,B2组较B1组改变更为明显。结论 本研究中两种TA对视网膜的影响不同。两种TA注射眼中可见随剂量加重的视网膜损害,不排除某些损害由难以彻底去除的溶媒成分引起。玻璃体内注射TA时应充分权衡其治疗效应与毒性效应。TA提取颗粒可能对视网膜光感受器细胞线粒体代谢功能具有潜在的保护或加强作用。     

氟尿嘧啶脂质体玻璃体注射防治增生性玻璃体视网膜病变的实验研究

目的 探讨氟尿嘧啶脂质体兔眼玻璃体内注射对增生性玻璃体视网膜病变的防治作用.方法 10只白色家兔,每只眼玻璃体内注射自体腹腔收集巨噬细胞制成增生性玻璃体视网膜病变动物模型.右眼为实验眼,玻璃体内注射氟尿嘧啶脂质体1次,浓度为1.6mg/0.1mL;左眼为空白对照,注射磷酸缓冲液.每周观察玻璃体视网膜病变发展程度.4周观察术后视网膜脱离发生率.结果 术后28天,实验组视网膜脱离发生率为30.00%(3/10),对照组为80.00%(8/10),差异有统计学意义.结论 玻璃体内注射氟尿嘧啶脂质体1次能有效地预防实验性增生性玻璃体视网膜病变的发生.     

透明质酸酶诱导玻璃体后脱离的实验研究

目的 研究透明质酸酶诱导玻璃体后脱离的安全性和有效性。方法 选取成年健康纯种新西兰白兔15只，随机分为A、B、C3组。随机选取每只兔的一眼为实验眼，另一眼为对照眼。A组玻璃体腔注入透明质酸酶5IU／0．1mL，B组透明质酸酶10IU／0．1mL，C组透明质酸酶20IU／0．1mL，对照组眼内注入0．1mL BSS。结果 A组术后所有眼均未见玻璃体后脱离；B、C组于术后第5周出现玻璃体后脱离，并且无出血、渗出或视网膜脱离等并发症发生。结论 浓度为10IU／0．1mL和20IU／0．1mL的透明质酸酶玻璃体腔注射后第5周可形成玻璃体后脱离，并且安全有效。     

基质金属蛋白酶-3在玻璃体切割术中的辅助作用研究

目的探讨玻璃体腔内注射基质金属蛋白酶-3(matrix metalloproteinase-3,MMP-3)对玻璃体切割术的辅助作用.方法将20只灰兔随机分成2组,右眼为实验眼,A组10眼玻璃体腔内注射平衡盐溶液(BSS)0.1mL,B组10眼注射MMP-3 0.1mL(10ng),注射后30min行玻璃体切割术;左眼为对照眼,玻璃体腔内注射等量BSS但不行玻璃体切割术.术毕摘除眼球行光镜、透射电镜及扫描电镜检查.结果A组兔眼后极部及赤道部内界膜均有多少不等的胶原纤维残留,且部分兔眼可见视网膜内界膜和感光细胞的损伤.B组兔眼内界膜面光滑平整、无任何物质残留.所有兔眼基底部视网膜面均见浓密的胶原纤维黏附.结论玻璃体腔内注射MMP-3可明显减少兔眼玻璃体切割术后玻璃体后皮质的残留,使手术更安全易行,可作为玻璃体切割术的辅助剂.     

低分子肝素缓释系统防治兔后发性白内障的实验研究

目的 探讨低分子肝素缓释系统防治兔后发性白内障的有效性和安全性.方法 采用前瞻性随机分组对照研究.以乳酸-羟基乙酸共聚物(PLGA)为载体采用冻干法制备低分子肝素缓释系统(LMWH DDS)并体外评价其缓释特性.将50只(50只眼)新西兰白兔分别行超声乳化透明晶状体吸除术,并随机均分为5组:A组术后生理盐水滴眼,B、C、D组术毕后房分别植入载药量为1.00 mg、0.50 mg、0.25 mg的LMWH DDS,E组植入不含药物的空白缓释系统;术后12周对术眼行裂隙灯显微镜、组织病理学以及电镜检查,并检测房水药物浓度和晶状体后囊膜湿重.术后房水闪光、房水细胞分级以及后囊膜混浊分级资料采用Kruskal-Wallis检验,房水药物浓度采用具有一个重复测量因素的两因素方差分析.结果 采用冻干法制备的LMWH DDS包封率为98.2%,体外释药方程拟合以零级方程为佳.术后B、C、D组炎症反应较A、E组显著减轻;术后12周A、B、C、D、E各组后囊膜混浊发生率分别为100%(10/10)、20%(2/10)、30%(3/10)、90%(9/10)、100%(10/10),后囊膜混浊分级评分组间比较差异均具有统计学意义(X~2=31.637,P=0.000),后囊膜湿重分别为(114.59±14.58)mg、(24.14±6.08)mg、(39.23±17.13)mg、(99.35±29.37)rag、(115.29±19.87)mg,组间比较差异均具有统计学意义(F=42.149,P=0.000);术后4周内B、C组房水中低分子肝素一直维持较高浓度(大于20 ms/L),D组浓度较低且不稳定;光镜和电镜下B、C组后囊细胞增生不活跃,未发现眼内毒性反应;术后均未见眼内出血现象.结论 以PLGA为载体采用冻干法制备的LMWHDDS具有良好的缓释性和组织相容性;其后房植入能明显减轻术后炎症反应,能安全、有效抑制后发性白内障的发生,且存在一定量效关系.     

LMWH inhibits anterior chamber inflammation after extra capsular lens extraction through down regulation of bFGF content in aqueous humor

AIM: To observe the changes of basic fibroblast growth factor (bFGF) content in anterior chamber before and after extra capsular lens extraction for investigating the mechanism of low molecular weight heparin (LMWH) inhibiting anterior chamber inflammation. METHODS: Eighty-four rabbits were randomly divided into control and experimental group, 42 rabbits in each group. Extra capsular lens extraction was done on unilateral eye in each rabbit. LMWH was perfused into anterior chamber by the concentration of 50U/mL at the end of operation in experimental group. The degrees of corneal edema, aqueous flare and fibrin were evaluated with slit lamp microscope on postoperative day 1, 3, 6, 15, 30, 45 and 60, respectively. Six eyes of each group were at each time point. Contents of bFGF in aqueous humor were determined by ELISA after animals were killed. Another six eyes were used for determining the base line level of bFGF in aqueous humor. RESULTS: The degrees of corneal edema, aqueous flare and fibrin in experimental group were significantly lighter than those in control group (P<0.01) on postoperative day 1, 3 and 6, respectively. No difference was showed between the two groups at other point time. Contents of bFGF in aqueous humor increased at the same time. bFGF content reached peak on postoperative day 1 in experimental group, while on postoperative day 6 in control group. Contents of bFGF in the two groups declined slowly after reaching peak. The bFGF content in control group were significantly higher than that in experimental group 1-30 days after surgery (P<0.05). No significant differences were shown between the two groups on postoperative day 45 and 60, respectively. CONCLUSION: Perfusion with LMWH by the concentration of 50U/mL can significantly reduce anterior chamber inflammation after extra capsular lens extraction in rabbits, which may be related to down regulation of bFGF content in aqueous humor.     

Effects of intravitreal dispase on vitreoretinal interface in rabbits

OBJECTIVE: To explore the efficacy and safety of dispase on the production of posterior vitreous detachment (PVD) following intravitreal injection at various concentrations for different exposure times in the rabbit eyes. METHODS: Sixty-four pigmented rabbits were assigned to two groups according to different combinations of concentrations of dispase and exposure times, namely group 1 (10, 5, or 1 U/ml for 30 min) and group 2 (0.25, 0.1, or 0.05 U/ml for one week). The control was established in both groups. One eye of each experimental rabbit was injected with dispase, and one eye of each control rabbit was injected with phosphate buffered saline. The presence of PVD and intraocular toxicity were observed by biomicroscope, macroexamination, and histology. RESULTS: None of the control eyes showed PVD. In group 1, PVD was present in 6 of 7 eyes in each sub-group. In group 2, all 7 eyes of 0.25 U/ml or 0.1 U/ml and 6 of 7 eyes of 0.05 U/ml showed PVD. Intraocular toxicity including inflammation in anterior chamber, vitreous haze, epiretinal membrane, and retinal damage were found in the experimental eyes with relatively higher concentrations of dispase. CONCLUSIONS: Although dispase has a definite effect on the induction of PVD in rabbits, its toxicity to retina also alerts us to the application in clinic. The intravitreal injection of dispase of 1 U/ml for 30 min may be acceptable.     

Vitrectomy with fluconazole infusion: retinal toxicity, pharmacokinetics, and efficacy in the treatment of experimental candidal endophthalmitis.

The aim of this study was to determine the retinal toxicity and intraocular pharmacokinetics of vitrectomy with fluconazole infusion in rabbit eyes and to study its efficacy in the treatment of experimental candidal endophthalmitis. The right eyes of 13 New Zealand White (NZW) rabbits were vitrectomized and infused with 20 mL of 0.2 mg/mL, 1 mg/mL, or 2 mg/mL of fluconazole. An electroretinogram (ERG) was performed on both eyes of each rabbit at different time points. The right eyes of 26 different NZW rabbits were vitrectomized and infused with 20 mL of 2 mg/mL of fluconazole. These rabbits were sacrificed, and their right eyes were enucleated at hours 2, 4, 8, and 24 after the operation, and the concentration of fluconazole in the vitreous was measured by highpressure liquid chromatography. Experimental candidal endophthalmitis was induced in the right eye of 42 other NZW rabbits. Twenty-six (26) of the eyes were then vitrectomized and infused with 20 mL of 2 mg/mL of fluconazole, and the other 16 rabbits served as control. Severity of ocular infection was graded from 0-4 at different time intervals, using an indirect ophthalmoscope. In the first group, ERG showed no significant difference between the experimental eyes and the control eyes--in all concentrations of fluconazole--for up to 3 months. In the second group, the intraocular concentration of fluconazole declined so rapidly that, as of 8 hours after operation, there was none in the vitreous cavity. In the third group, significantly less vitreous opacity was found in the treated eyes on days 3 and 6. However, the difference ceased to be apparent on day 15. Our study suggests that there is no retinal toxicity resulting from vitrectomy with a 2 mg/mL fluconazole infusion, and that it is temporally effective in the treatment of experimental candidal endophthalmitis.     

兔玻璃体内注射聚N-异丙基丙烯酰胺-聚氧化乙烯纳米粒的眼内毒理学效应

目的:评估玻璃体腔内注射新型缓释给药载体聚N-异丙基丙烯酰胺-聚氧化乙烯(PNIPAAm-PEO)纳米粒的眼内毒理学效应。方法:玻璃体腔注射不同浓度(1mg/0.1mL,2mg/0.1mL,3mg/0.1mL,4mg/0.1mL)的PNIPAAm-PEO纳米稀释液后于不同时间点行裂隙灯、检眼镜、视网膜电图以及组织病理学检测。对照组注射0.1mL无菌生理盐水。将所用不同浓度稀释液局部点眼,观察局部组织的刺激反应。结果:兔眼角结膜对检测浓度范围内的PNIPAAm-PEO有良好耐受性,眼部无刺激症状。玻璃体腔内注射1mg和2mg组未见明显视网膜毒性反应。3mg组眼底检查无异常,ERG-b波1~3d下降幅度>30%,第7~14d略有恢复;第14d光镜下视网膜部分感光细胞外节间隙增宽,外丛状层以内结构空泡变性,细胞排列正常;电镜下各层均有较明显的结构改变,广泛的细胞水肿和空泡变性,细胞间隙增宽,感光细胞膜盘结构基本正常。4mg组ERG-b波波幅下降>30%;第1~14d组织病理学观察均有明显视网膜结构破坏,广泛空泡变性,部分感光细胞的盘膜崩解,层状结构紊乱、模糊不清。结论:PNIPAAm-PEO纳米粒的眼部耐受性良好,具有用作眼部给药载体的潜力,但大剂量使用时应注意眼部安全性问题。     

蛇毒纤溶酶诱导兔眼玻璃体后脱离的实验研究

目的观察蛇毒纤溶酶是否可以诱导兔眼玻璃体后脱离（PVD）,并评价其对视网膜的毒性作用。方法根据随机数字表法将24只新西兰白兔分为A、B、C、D组,每组6只。左眼玻璃体腔注射0.1mL生理盐水作为对照。右眼玻璃体腔分别注入1000U/mL（商品单位）的蛇毒纤溶酶0.04、0.05、0.08、0.1mL,术后1、3、7d通过裂隙灯、间接检眼镜检查,观察眼前后节的变化。术后7d通过组织病理学检查,观察药物注入后是否诱发PVD,并评价其对视网膜结构的影响。结果术后7d对照眼无PVD形成,光学显微镜下见各实验组均有不同程度的部分性PVD形成。A、B、C组的视网膜结构与对照组比较无明显改变;D组可见局限性视网膜内界膜溶解破坏,局部视网膜隆起变薄及脉络膜下渗出的毒性改变。A组和D组的扫描电镜结果与光学显微镜一致。随着玻璃体腔蛇毒纤溶酶注射剂量的增加,玻璃体液化程度加大,PVD的范围也加大。结论兔眼玻璃体腔注射适当剂量的蛇毒纤溶酶,在术后7d可以诱导部分性PVD的形成,且视网膜形态无明显改变。大剂量应用时可见视网膜结构的毒性改变。     

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。     

聚乙烯醇（PVA）水凝胶填充兔玻璃体腔的安全性及有效性研究

目的　评价30 g·L^-1聚乙烯醇（polyvinyl alcohol,PVA）水凝胶在兔玻璃体腔内长期填充的安全性与有效性。方法　将新西兰白兔12只随机分为2组:PVA水凝胶组（PVA组）6只、BSS组6只。2组兔右眼行三通道玻璃体切割术,切除玻璃体后分别填充PVA水凝胶和BSS溶液。术后行裂隙灯、眼底镜、眼压、B超和眼底照相检查;术后90 d、180 d行视网膜电流图（electroretinogram,ERG）检查,同时处死兔并摘出眼球,收集眼内PVA水凝胶后行流变学检查,眼球送病理学检查。结果　至观察终期PVA组与BSS组术眼的角膜、前房等均无明显异常;PVA组有2眼并发白内障、BSS组有1眼并发白内障,2组术眼均未见玻璃体积血、混浊、增殖,视网膜脱离,脉络膜脱离等并发症出现。眼压情况:术前及术后3 d、7 d、14 d、30 d、60 d、90 d和180 d,两组间各时间点眼压比较差异均无统计学意义（均为P>0.05）。ERG检查提示2组术眼SkotERG和PhotERG的a波、b波峰值与术前相比,差异均无统计学意义（均为P>0.05）,两组间比较差异亦均无统计学意义（均为P>0.05）。眼球固定切片和HE染色,光镜下显示:2组术眼视网膜全层结构完整,内丛状层和外丛状层连续,内、外核层细胞排列整齐,视网膜全层细胞未见明显炎症、变性、坏死等改变。电镜下观察显示:术后90 d视网膜色素上皮细胞线粒体轻度水肿、结构欠清,周围有PVA高分子物附着;而术后180 d线粒体细胞水肿明显加重、结构更加模糊。PVA水凝胶在术后90 d玻璃体腔内仍填充较饱满,未见明显降解,黏弹性能未见明显改变,而在术后180 d玻璃体腔内的PVA水凝胶水样物增多,出现明显降解,黏弹性能显著降低。结论　30 g·L^-1PVA水凝胶在体内有良好的生物相容性和视网膜支撑功能,但长期填充后容易被降解。     

Safety of intravitreal quinupristin/dalfopristin in an animal model

AIM: To determine whether different intravitreal doses of quinupristin/dalfopristin lead to electroretinographic or histological changes in the rabbit retina over one month period after injection. METHODS: Eighteen New Zealand white rabbits were divided into three treatment groups (groups 1 to 3) and different intravitreal doses of quinupristin/dalfopristin were tested in each group. The right eye was injected with the drug and the left eye received intravitreal injection of 5% dextrose water and served as control eye. The doses delivered to each group were 0.1 mg/0.1 mL, 1 mg/0.1 mL and 10 mg/0.1 mL. Simultaneous, bilateral, dark-adapted electroretinography and clinical images of both eyes were obtained in all groups before injection (baseline) and after 7, 14, 21 and 28d, followed by enucleation for histological examination. RESULTS: Subjects in the group 1 showed no signs of toxicity in the electroretinogram when compared with groups 2 and 3 (Kruskall-Wallis test, P=0.000). By day 7, no electrical response to light stimuli was recorded in the treated eyes in groups 2 and 3, consistent with severe damage due to retinal toxicity. Light microscopy revealed no significant histopathological changes in the group 1, while rabbits in groups 2 and 3 had signs of granulomatous inflammation in most cases. CONCLUSION: Intravitreal 0.1 mg/0.1 mL doses of quinupristin/dalfopristin do not lead to electroretinographic or histological signs of retinal toxicity compared with 1 mg/0.1 mL and 10 mg/0.1 mL in this rabbit model.     

低分子肝素下调房水bFGF含量抑制晶状体囊外摘除术后前房炎症

目的:观察房水中碱性成纤维细胞生长因子(basic fi-bro blast growth factor,bFGF)含量的变化,探讨低分子肝素(low molecular weight heparin,LMWH)抑制晶状体摘除术后前房炎症的机制。方法:家兔84只随机分为对照组和实验组,每组42只,行单眼透明晶状体囊外摘除术。实验组手术结束时用浓度为50kU/L的LMWH进行前房灌注。分别于术后1,3,6,15,30,45,60d每组各取6只家兔,裂隙灯显微镜下对角膜水肿、房水混浊及前房纤维蛋白渗出的程度进行观察和分级,然后处死动物,抽取房水用Elisa法测定bFGF的含量。另选6只健康家兔测定前房bFGF含量作为基线值。结果:术后1～6d,实验组角膜水肿、房水混浊及前房纤维蛋白渗出的程度明显轻于对照组(P<0.01),15d后两组比较无差异。术后实验组和对照组房水bFGF含量同时升高,实验组1d达峰值,而对照组6d达峰值;达峰值后两组bFGF含量均缓慢下降。术后1～30d对照组bFGF含量明显高于实验组(P<0.05),45d后两组比较无显著性差异。结论:应用浓度为50kU/L的LMWH前房灌注能显著降低兔眼晶状体囊外摘除术后前房炎症反应,其机制可能与房水中bFGF含量下调有关。     

纤溶酶和透明质酸酶诱导猪玻璃体后脱离的比较研究

目的：研究纤溶酶和透明质酸酶诱导猪玻璃体后脱离（PVD）的有效性和安全性,比较两种酶单独应用和联合应用的效果。 方法：小型猪15只随机分为A,B,C三组,每组5只,随机选取1只眼为实验眼,对侧眼为对照眼。三组实验眼玻璃体腔分别注射50U（0.1mL）透明质酸酶、0.5U（0.1mL）纤溶酶和0.5U（0.05mL）纤溶酶加50U（0.05mL）透明质酸酶,对照眼均注射平衡盐溶液（BSS）0.1ml。注药后进行裂隙灯、直、间接检眼镜、眼B超、视网膜电图（ERG）等检查,7d后摘除眼球进行光镜、透射电镜、扫描电镜检查。 结果：B超检查显示A组有1只实验眼、B组有两只实验眼于注药后1d观察到部分性PVD,C组有1只实验眼于注药后1h观察到部分性PVD。B超、光镜和扫描电镜检查显示注药后7dA组和B组实验眼均见部分性PVD,C组实验眼均见完全性PVD,对照眼未见PVD。实验及对照眼注药前、后ERGa波、b波波幅均无显著性差异,光镜及透射电镜检查未见视网膜损害。 结论：0.5U纤溶酶和50U透明质酸酶单独及联合应用均可快速、安全、有效地诱导猪眼玻璃体后脱离,且联合用药较单独用药诱导PVD更快速、更有效。