腺病毒载体介导的单纯疱疹病毒胸苷激酶／丙氧鸟苷系统抑制晶状体后囊膜混浊的研究

背景晶状体后囊膜混浊（PCO）目前尚无有效的防治途径。目的研究腺病毒载体介导的单纯疱疹病毒胸苷激酶（HSV-tk）／丙氧鸟苷（GCV）系统对PCO的抑制作用。方法选取新西兰白兔12只,用电脑随机选号法随机分为BSS＋BSS组、BSS＋GCV组、HSV-tk＋BSS组及HSV-tk＋GCV组,每组3只。兔眼行晶状体超声乳化摘出术,术中依据分组情况分别在晶状体囊袋中注入0．1mlBSS或携带有HSV-tk基因的腺病毒载体,术后12h分别在BSS＋BSS组和HSV-tk＋BSS组兔眼前房注入0．1mlBSS,BSS＋GCV组及HSV-tk＋GCV组以同样的方法注入GCV,每日1次,共3次。术后裂隙灯下观察眼前节情况,PCO分级按照Couderc的方法。术后4周摘除兔眼,采用Miyake-Apple法观察PCO情况,显微镜下取出晶状体囊袋后以电子天平称出整个囊袋湿质量,并行晶状体囊袋的组织学检查。结果术后1～3d各组均可见角膜轻度水肿与房水混浊,2周内基本恢复正常。术后4周,HSV-tk＋GCV组PCO明显轻于其他3组,差异均有统计学意义（H=2．647、H=2．939、H=2．884,P〈O．05）,而BSS＋BSS组、BSS＋GCV组、HSV-tk＋BSS组组间的差异均无统计学意义（H=0．631、H=0．924、H=0．589,P〉0．05）。Miyake-Apple法观察显示,HSV-tk＋GCV组PCO面积与密度小于其他3组,晶状体囊袋湿质量也明显轻于其他3组,差异均有统计学意义（q=9．93、q=10．15、q=10．07,P〈O．05）,BSS＋BSS组、BSS＋GCV组、HSV-tk＋BSS组组间差异均无统计学意义（q=0．22、q=0．07、q=015,P〉0．05）。囊袋组织学检查提示HSV-tk＋GCV组可见少量赤道部晶状体上皮细胞（LECs）增生并向后囊膜迁移,在囊袋外周形成稀薄的soemmering环,在中央部无细胞和皮质,或仅形成单细胞层纤维膜。BSS＋BSS组、BSS＋GCV组、HSV—tk＋BSS组可见大量赤道部LECs增生和迁移,在囊袋外周部soemmering环稠厚,在中央部形成多细胞层纤维膜。结论腺病毒载体介导的HSV-tk／GCV系统能有效抑制PCO。     

腺病毒载体介导的单纯疱疹病毒胸苷激酶基因/丙氧鸟苷体系对晶状体上皮细胞的作用

目的：观察腺病毒载体介导的单纯疱疹病毒胸苷激酶（herpes simplex virus thymidine kinase,HSV-tk）基因／丙氧鸟苷（ganciclovir,GCV）体系对体外培养的牛晶状体上皮细胞的杀伤效应,并初步探讨晶状体上皮细胞死亡的机制。方法：利用携带HSV－tk基因的重组腺病毒载体adenoviral vector(ADV)/HSV-tk,感染体外培养的牛晶状体上皮细胞后用GCV治疗,并观察疗效。以切除E1区的空腺病毒载体ADV／Empty作为对照。以电镜、TUNEL法及吖啶橙－溴化乙啶染色法检测晶状体上皮细胞的凋亡及坏死情况。结果：GCV在体外对感染ADV／HSV－tk的牛晶状体上皮细胞有明显的杀伤作用,且具有旁观者效应,而对转染了ADV／Empty的细胞则无显著的毒性。GCV的杀伤效应随剂量的增大及时间延长而增强。导入HSV－th基因的晶状体上皮细胞出现明显的细胞凋亡现象,而且细胞的凋亡率（t=7.28,P＜0．01）及坏死率（t=14.72,P＜0．001）显著高于对照组。结论：腺病毒载体可将HSV-tk基因转导入牛晶状体上皮细胞中;GCV可有效杀伤表达HSV－tk的晶状体上皮细胞;HSV－tk/GCV体系引发的细胞死亡可能与亡及坏死两种机制有关;腺病毒载体介导的HSV－tk/GCV体系有可能成为后发性白内障的有效治疗方法。     

慢病毒介导的单纯疱疹病毒胸苷激酶基因/丙氧鸟苷体系抑制人晶状体上皮细胞的研究

目的探讨慢病毒介导的单纯疱疹病毒胸苷激酶基因／丙氧鸟苷体系（HSV—tk／GCV）对人晶状体上皮细胞（LECs）系的杀伤效应的机制。方法HSV—tk基因和增强型绿色荧光蛋白（EGFP）报告基因共表达的慢病毒感染细胞为试验组,仅表达EGFP的慢病毒感染细胞和正常细胞为对照组。流式细胞仪检测病毒的转染效率,荧光显微镜观察及基因组PCR和RT-PCR检测基因在LECs内表达,DNA ladder和电镜观察该系统对LECs的杀伤作用,检测HSV—tk／GCV系统的浓度时间依赖性和旁观者效应。结果HSV—tk整合入LECs并高效表达。10～25μg／ml的GCV能明显诱导转染HSV—tk的细胞凋亡或坏死,且随GCV浓度升高和作用时间延长效应增强,且存在明显的旁观者效应,而对照组细胞无显著改变。当GCV浓度〉25μg／ml,对照组细胞的增殖也被显著抑制。结论GCV可高效杀伤表达HSV-tk的LECs,且旁观者效应显著增强了HSV—tk／GCV系统的杀伤效果。HSV—tk和EGFP共表达的慢病毒载体能高效稳定转染LECs。     

基质金属蛋白酶抑制剂抑制兔晶状体后囊膜混浊的研究

目的 观察基质金属蛋白酶(MMP)抑制剂对兔晶状体后囊膜混浊的抑制作用和对眼内组织的毒性.方法 实验研究.选用新西兰白兔行超声乳化晶状体吸除术,用不同浓度的MMP抑制剂GM6001溶液(实验1组:100 μmol/L,实验2组:200 μmol/L,实验3组:500 μmol/L)和GM6001阴性对照液(500 μmol/L)进行术毕及术后隔日晶状体囊袋内灌注3次,观察术后第12周内后囊膜混浊情况,同时观察药物对眼前房反应、眼压、角膜内皮、虹膜、睫状体和视网膜的影响和毒性.采用四格表确切概率法分析使用GM6001后前房反应和对后囊膜混浊的抑制作用;采用单因素方差分析法分析GM6001对眼压的影响.结果 裂隙灯显微镜下观察,可见术后12周对照组后囊膜混浊明显,实验1组后囊膜混浊较对照组轻,实验2组和3组均无后囊膜混浊(P=0.007);病理学结果显示:对照组和实验1组后囊膜表面有多层排列紊乱的上皮细胞和成纤维细胞,而实验2组和3组后囊膜表面几乎无细胞生长;前房反应轻:用药2 d实验组和对照组兔眼前房闪光情况比较,差异无统计学意义(P=0.380);对眼压的影响:实验组与对照组用药2 d(F=0.642,P=0.597)、7 d(F=0.179,P=0.909)眼压比较,差异均无统计学意义;用药7 d,实验3组角膜内皮细胞呈规则的六边形,无变形脱落,与对照组眼角膜内皮细胞形态无明显差别;光镜观察发现对虹膜、睫状体和视网膜均无明显毒性.结论 MMP抑制剂可明显抑制兔眼超声乳化晶状体吸除术后晶状体后囊膜混浊的发生,对眼内组织无明显毒性,安全有效.

Abstract：

Objective To determine whether matrix metalloproteinase (MMP) inhibitor can provide therapeutic effects for rabbits posterior capsule opacification in vivo and to observe the side effects of this drug on surrounding intraocular structures. Methods Experimental research. New Zealand white rabbits were undertaken phacoemulsification operation. GM6001 at different concentrations ( 100,200 and 500 μmol/L)and GM6001 negative control liqueur were infused into the capsule bags of the rabbits at the end of operation and two days after the operation. The incidence of posterior capsule opacification was assessed and the histological sections of posterior capsules were observed under microscope 12 weeks after the surgery. The anterior chamber response was observed on day 2 post-operatively. The changes of intraocular pressure were measured by day 2 and day 7. Corneal endothelial cells were observed under scanning electron microscopeand iris, ciliary body and retina were observed under microscope on day 7. Results GM6001 significantly prevented posterior capsule opacification (P=0. 007 ). No opacification occurred on the rabbit posterior capsule in eyes with 200 and 500μmol/L GM6001 on week 12 post-operatively in vivo. No cells were found on posterior capsule in 500 μmol/L group, whereas lens epithelial cells and fibroblasts were found in the controls under microscope. No difference of anterior chamber flare between the eyes with GM6001 at different concentrations and the control group (P=0. 380) by day 2 after the operation. The intraocular pressure in eyes with GM6001 was the same as that in the control 2-days ( F = 0. 642, P = 0. 597 ) and 7-days ( F =0. 179 ,P =0. 909) post-operation. The corneal endothelial cells in eyes with 500 μ mol/L GM6001 arranged regularly and did not show any difference from that in the control eyes under scanning electron microscope 7-day after the operation. The iris, ciliary body and retina in eyes with 500 μmol/L GM6001 were normal in appearance 7-day after the operation. Conclusions MMP inhibitor can prevent posterior capsule opacification effectively in rabbits in vivo and does not cause damage to surrounding intraocular structures,suggesting that MMP inhibitor may become a medication used for the prevention of lens posterior capsule opacification.     

基质金属蛋白酶抑制剂抑制兔晶状体后囊膜混浊的研究

Objective To determine whether matrix metalloproteinase (MMP) inhibitor can provide therapeutic effects for rabbits posterior capsule opacification in vivo and to observe the side effects of this drug on surrounding intraocular structures. Methods Experimental research. New Zealand white rabbits were undertaken phacoemulsification operation. GM6001 at different concentrations ( 100,200 and 500 μmol/L)and GM6001 negative control liqueur were infused into the capsule bags of the rabbits at the end of operation and two days after the operation. The incidence of posterior capsule opacification was assessed and the histological sections of posterior capsules were observed under microscope 12 weeks after the surgery. The anterior chamber response was observed on day 2 post-operatively. The changes of intraocular pressure were measured by day 2 and day 7. Corneal endothelial cells were observed under scanning electron microscopeand iris, ciliary body and retina were observed under microscope on day 7. Results GM6001 significantly prevented posterior capsule opacification (P=0. 007 ). No opacification occurred on the rabbit posterior capsule in eyes with 200 and 500μmol/L GM6001 on week 12 post-operatively in vivo. No cells were found on posterior capsule in 500 μmol/L group, whereas lens epithelial cells and fibroblasts were found in the controls under microscope. No difference of anterior chamber flare between the eyes with GM6001 at different concentrations and the control group (P=0. 380) by day 2 after the operation. The intraocular pressure in eyes with GM6001 was the same as that in the control 2-days ( F = 0. 642, P = 0. 597 ) and 7-days ( F =0. 179 ,P =0. 909) post-operation. The corneal endothelial cells in eyes with 500 μ mol/L GM6001 arranged regularly and did not show any difference from that in the control eyes under scanning electron microscope 7-day after the operation. The iris, ciliary body and retina in eyes with 500 μmol/L GM6001 were normal in appearance 7-day after the operation. Conclusions MMP inhibitor can prevent posterior capsule opacification effectively in rabbits in vivo and does not cause damage to surrounding intraocular structures,suggesting that MMP inhibitor may become a medication used for the prevention of lens posterior capsule opacification.     

基质金属蛋白酶抑制剂抑制兔晶状体后囊膜混浊的研究

Objective To determine whether matrix metalloproteinase (MMP) inhibitor can provide therapeutic effects for rabbits posterior capsule opacification in vivo and to observe the side effects of this drug on surrounding intraocular structures. Methods Experimental research. New Zealand white rabbits were undertaken phacoemulsification operation. GM6001 at different concentrations ( 100,200 and 500 μmol/L)and GM6001 negative control liqueur were infused into the capsule bags of the rabbits at the end of operation and two days after the operation. The incidence of posterior capsule opacification was assessed and the histological sections of posterior capsules were observed under microscope 12 weeks after the surgery. The anterior chamber response was observed on day 2 post-operatively. The changes of intraocular pressure were measured by day 2 and day 7. Corneal endothelial cells were observed under scanning electron microscopeand iris, ciliary body and retina were observed under microscope on day 7. Results GM6001 significantly prevented posterior capsule opacification (P=0. 007 ). No opacification occurred on the rabbit posterior capsule in eyes with 200 and 500μmol/L GM6001 on week 12 post-operatively in vivo. No cells were found on posterior capsule in 500 μmol/L group, whereas lens epithelial cells and fibroblasts were found in the controls under microscope. No difference of anterior chamber flare between the eyes with GM6001 at different concentrations and the control group (P=0. 380) by day 2 after the operation. The intraocular pressure in eyes with GM6001 was the same as that in the control 2-days ( F = 0. 642, P = 0. 597 ) and 7-days ( F =0. 179 ,P =0. 909) post-operation. The corneal endothelial cells in eyes with 500 μ mol/L GM6001 arranged regularly and did not show any difference from that in the control eyes under scanning electron microscope 7-day after the operation. The iris, ciliary body and retina in eyes with 500 μmol/L GM6001 were normal in appearance 7-day after the operation. Conclusions MMP inhibitor can prevent posterior capsule opacification effectively in rabbits in vivo and does not cause damage to surrounding intraocular structures,suggesting that MMP inhibitor may become a medication used for the prevention of lens posterior capsule opacification.     

阿霉素药物缓释系统抑制人工晶状体植入术后后囊膜混浊的实验研究

目的 探讨阿霉素药物缓释系统(ADM-DDS)对兔眼人工晶状体植入术后后囊膜混浊(PCO)的抑制作用及其毒副作用,为临床应用提供实验依据。方法 自制聚乳酸(PLA)为载体的眼内植入型ADM-DDS,内含ADM 22μg。采用兔眼晶状体囊外摘出联合人工晶状体植入术的动物模型,术中将ADM-DDS植入15只兔眼晶状体囊袋内。术后临床常规检查,第4周行病理组织学及电镜检查。结果 实验组与对照组比较,晶状体后囊膜混浊减轻(t=2,P<0.01),Soemmering环面积减小(t=20.51,P<0.01),兔眼晶状体上皮细胞(RLECs)细胞核固缩坏死,胞浆凝集、空泡变性。两组之间的眼压、角膜内皮细胞形态及密度以及光镜下角膜、虹膜、睫状体、视网膜组织均无差异。结论 兔眼内植入ADM-DDS通过ADM缓释作用抑制了人工晶状体植入术后RLECs的增殖。ADM-DDS对兔眼角膜、虹膜、睫状体及视网膜无明显毒性。以PLA为载体的DDS将有可能成为临床上药物预防PCO的一种有效而安全的给药途径。     

5-Fu纳米粒涂层人工晶状体抑制兔晶状体后囊膜混浊的实验研究

目的 制备5-Fu纳米粒涂层人工晶状体(IOL)并探讨其对兔晶状体后囊膜混浊的抑制作用的有效性和可行性.方法 通过低能离子束表面氟离子注入技术使5-Fu纳米粒与IOL表面交联黏附形成涂层.取新西兰大白兔40只,随机分为A、B两组,每组20只,对左眼行超声乳化透明晶状体吸出术,对照组为A组,植入普通IOL;实验组为B组,植入5-Fu纳米粒涂层IOL.术后行裂隙灯显微镜、组织病理学及电镜检查.所有数据用SAS统计软件处理,前房闪光和晶状体后囊膜中央视区混浊程度均用Kruskal-Wallis秩和检验进行分析.结果 前房炎性反应:B组的前房闪光轻于A组,差异有统计学意义(x~2=11.245,P=0.024).两组兔眼的前房反应均在术后3 d至1周内缓解.晶状体后囊膜混浊:B组晶状体后囊膜的混浊程度轻于A组,差异有统计学意义(x~2=10.304,P=0.016).光学显微镜行组织病理学检查:A组眼内炎性反应较轻,B组无明显眼内炎性反应表现,A、B两组角巩缘结构及组织均无病理损害.扫描电子显微镜检查:A组见晶状体上皮细胞增生现象,B组未见明显晶状体上皮细胞增生.结论 兔眼透明晶状体超声乳化吸出术后植入5-Fu纳米粒涂层IOL,可有效抑制晶状体后囊膜混浊的发生,眼内毒性较小.     

丝裂霉素抑制后囊膜混浊的实验研究

目的 探讨丝裂霉素抑制后囊膜混浊的有效浓度及可能造成的眼损害和临床应用的可行性。方法 大耳白兔30只,随机分为6组,每组5只,施行晶状体囊外摘出术。对照组用BSS 0．3ml注入囊袋内进行水分离,实验组分别给予0．01％,0．02％,0．03％,0．04％,0．05％丝裂霉素0．3ml注入囊袋内进行水分离。术中均用玻璃酸钠先行保护角膜。随访3个月,处死动物,手术显微镜及光镜观察后囊膜混浊情况、角膜透明度及炎症反应。结果 随访3个月发现,后囊膜混浊多见于术后2个月,时间越长,混浊范围越大。随用药质量浓度增加,后囊膜混浊发生率及严重程度下降,未发现角膜、虹膜及睫状体损伤。结论 囊袋内应用丝裂霉素,并用玻璃酸钠保护角膜内皮,可减少后囊膜混浊发生率且无邻近眼组织损伤。     

柔红霉素预防晶状体后囊膜混浊的实验研究

目的：通过动物实验探讨柔工霉素预防白内障术后的后囊膜混浊的作用及临床应用价值。方法：采用柔红霉素5．0μg/ml,7.5μg/ml两种浓度在兔眼晶状体囊外摘除术中行囊袋内灌注5分钟,通过裂隙灯显微镜观察其术后反应。术后3个月取眼球做病理切片观察组织的毒性反应。结果：随访3个月,用药后发障的发生率明显减,水发现角膜,葡萄膜及视网膜的毒性反应。结论：柔红霉素术中一次性囊袋内灌注,可养活后囊混浊的发生率,并对周围组织无损伤,安全,有效,方便使红霉素在混浊预防方面有临床应用价值。     

白内障摘除人工晶状体植入术后晶状体后囊膜混浊的基础研究

晶状体后囊膜混浊是目前白内障摘除人工晶状体植入术后影响视功能恢复的主要并发症 ,其发生与手术残留的晶状体上皮细胞增殖有关。为了预防该并发症的发生 ,研究其发病机制成为眼科临床的重要任务。许多眼科医生进行了大量的基础研究工作 ,力求从根本上解决白内障摘除人工晶状体植入术后晶状体后囊膜混浊的发生。正常晶状体上皮细胞的生物学特性人眼晶状体起源于外胚层 ,由晶状体囊膜、囊膜下晶状体上皮细胞及其产物 ,即晶状体纤维组成。晶状体上皮细胞为单层立方上皮细胞 ,紧密贴附于前囊膜的内表面 ,与下方的晶状体纤维疏松连接。晶状体上…     

晶状体后囊膜混浊的研究方法及细胞生物学研究进展

晶状体后囊膜混浊(PCO)是现代白内障囊外摘除联合人工晶状体植入术术后引起视力下降的常见,有多种方法用于研究后囊膜混浊,但各有利弊.细胞调节系统在后囊膜混浊的形成发挥重要作用.本文就后囊膜混浊的不同研究方法及与后囊膜混浊有关的细胞生物学调节方式进行综述,展望防治PCO的前景.     

双氯芬酸钠抑制兔后囊膜混浊的实验研究

目的 探讨双氯芬酸钠抑制兔后囊膜混浊(posterior capsule opacification,PCO)的安全性和有效性.方法 20只大耳白兔(40眼)随机分为空白对照组(A组),1 g·L-1双氯芬酸钠滴眼液组(B组),1g·L-1、5 g·L-1、10g· L-1双氯芬酸钠灌注液组(分别为C、D、E组),双眼均行透明晶状体囊外摘出术,B组术后使用1g·L-1双氯芬酸钠滴眼液滴眼,术中不进行双氯芬酸钠滴眼液前房灌注;C、D、E组术中分别使用1g·L-1、5g·L-1、10g· L-1双氯芬酸钠滴眼液前房灌注,术后使用1g·L-1双氯芬酸钠滴眼液滴眼.术后1周观察角膜及前房反应;1个月后用裂隙灯及检眼镜检查后囊膜情况,进行PCO分级;术后1个月,HE染色观察后囊膜病理改变情况,并用免疫组织化学SABC法检测后囊膜增殖的晶状体上皮细胞PCNA表达情况.结果 A、B组术后1周左右开始形成PCO并逐渐加重,1个月后出现明显PCO,C、D、E组PCO出现方式与A组相同,但出现时间晚、程度较轻.术后1个月A、B组PCO程度较C、D、E组重,差异均有统计学意义(均为P＜0.05);A、B组之间和C、D、E组之间差异均无统计学意义(均为P＞0.05).术后1个月,各组后囊膜晶状体上皮细胞均有PCNA阳性表达,且PCNA阳性细胞数随药物浓度的提高而减少,分别为15.63±1.92、12.87±1.81、8.63±0.92、5.50±1.31、2.00±0.76.与A组相比,B、C、D、E组术后后囊膜PCNA阳性细胞数明显减少,差异均有统计学意义(均为P＜0.05);B、C、D、E组间PCNA阳性上皮细胞数差异有显著统计学意义(P＜0.01).结论 术中双氯芬酸钠滴眼液前房灌注联合术后双氯芬酸钠滴眼液滴眼可有效延缓PCO的发生,对眼前段无明显毒性作用.     

直角边缘人工晶状体预防兔后囊膜混浊的实验研究

目的探讨直角边缘人工晶状体（intraocular lens，IOL）预防后囊膜混浊（posterior capsule opacification，PCO）的作用。方法30只新西兰兔进行超声乳化晶状体摘出联合囊袋内IOL植入术后，随机植入Crane OV-55CP、Crane OV-55C、Alcon TYPE 5C 3种IOL之一。观察术后并发症和PCO情况。术后3月行光镜和透射电镜检查，观察晶状体后囊膜的形态学变化。结果术后3月Crane OV-55CP组的PCO程度比Crane OV-55C和Alcon TYPE 5C组轻（P〈0．05），各组Soemmefing环形成程度无差异（P〉0．05）。病理学检查发现Crane OV-55CP组兔赤道部增生的晶状体上皮细胞在人工晶状体的直角边缘处受到了阻挡。Crane OV-55C和Alcon TYPE 5C组大量晶状体上皮细胞迁移至后囊膜。结论直角边缘IOL延缓了兔PCO的发生、发展，是预防PCO简便安全有效的方法。     

丝裂霉素-C眼内应用抑制后囊膜混浊的实验研究

目的 通过动物实验，研究眼内应用浓度为0．2mg／ml的丝裂霉素-C(MMC)对于术后后囊膜混浊的抑制作用。方法 将32只实验动物随机分为A，B，C，D四组。所有的实验动物均进行晶状体超声乳化摘除术。A组为对照组，B组术中应用0．2mg／ml的MMC溶液作水分离，C组术中将混有0．2mg／mlMMC的粘弹剂注入囊袋中，D组将MMC溶于配好的灌注液，术中应用。术后进行术眼裂隙灯检查、房水免疫球蛋白测定及角膜内皮细胞分析，术后1月进行术眼后囊照相。结果 术后1天和1周，D组角膜水肿的例数及持续时间均明显高于其他三组。角膜内皮细胞分析显示D组的角膜内皮数量明显低于其余三组。术后1天、1周1月时D组房水中IgG含量明显高于同时期的其余三组。其余三组无显著性差异。术后1月术眼后囊照相可见A组中央后囊明显混浊，B、C、D组中央后囊清亮。结论 实验显示眼内应用0．2mg／ml的MMC明显抑制了后囊膜混浊的发展。尽管眼内应用0．2mg／ml的MMC可以导致眼内组织毒性反应，但通过用药方法的改进和保护措施的加强是可以有效避免或减轻的。     

不同设计人工晶状体植入术后3年后囊膜混浊的研究

目的研究不同材料和不同设计的人工晶状体植入术后3年的后囊膜混浊(posterior capsular opacification,PCO)发生率及PCO形态。方法回顾性研究132眼老年性白内障患者,由同一医生进行超声乳化联合人工晶状体(in-traocular lens,IOL)植入术,根据IOL的不同分为4组:Storz Hydroview H60M组(33眼),Silicone折叠式硅胶IOL组(29眼),AcrySof三片式IOL组(36眼)和聚甲基丙稀酸甲酯(poly-methyl methacrylate,PMMA)组(34眼)。术后3年随访患眼的最佳矫正视力(best corrected visual acuity,BCVA),扩瞳后采集PCO数码图像,分析不同IOL组PCO的形态及PCO发生率。结果各种IOL的PCO形态各异,H60M组和AcrySof组分别有10眼和15眼后囊形成皱折,而Silicone和PMMA组为片状混浊。虽然各组BCVA和BCVA下降率差异没有显著性(P>0.05),但PCO发生率差异有非常显著性,分别是AcySof组5.6%,Silicone组30.3%,H60M组31%和PMMA组55.9%。结论AcrySof疏水丙烯酸酯三片式折叠IOL,有直角边缘设计,术后3年能明显降低PCO的发生。     

眼内应用丝裂霉素C抑制后囊膜混浊的组织病理学研究

目的：研究兔晶状体超声乳化术中眼内应用0．2mg／ml的丝裂霉素C(mitomycin-C，MMC)对术后后囊膜混浊的抑制作用，并比较不同给药方式对眼毒性的差异。方法：将32只新西兰白化兔随机分为A、B、C、D4组，进行晶状体超声乳化摘除术。A组为空白对照组，B组用0．2mg／ml的MMC溶液在环形撕囊后作水分离，C组在术中将混有MMC(0．2mg／ml)的粘弹剂注入空的囊袋中，D组将MMC(0．2mg／ml)溶于配好的灌注液中，在手术中应用。术后1个月对术眼进行组织病理学检查。结果：术后1个月时光镜下A组中赤道部及中央后囊膜均可见晶状体上皮细胞的明显增生、移行及大量排列紊乱的成纤维细胞和胶原纤维。B、C、D三组中可见赤道部少量残留的晶状体上皮细胞及皮质，中央后囊的表面未见品状体上皮细胞、成纤维细胞或珍珠样小体。透射电镜下，D组中虹膜上皮、睫状体上皮及视网膜各层均发生了不同程度超微结构的损伤，A、B、C三组间未见明显异常。结论：眼内应用0．2mg／ml的MMC明显抑制后囊膜混浊的发展。尽管眼内应用0．2mg／ml的MMC可以导致眼内组织的毒性，但通过改进用药方法和加强保护措施，可有效地避免或减少药物的眼毒性。在应用于临床之前，仍需进一步动物实验研究。     

连续环形撕囊术抑制后囊膜混浊的实验研究

目的：搪塞连续环形撕囊术（ＣＣＣ）对白内障囊外摘除术后晶体后囊膜混浊的影响。方法：将２４只白色家兔随机平均分为三个时间组,每只家兔又按双眼术中前切开法的不同随机分为ＣＣＣ组和开罐式截囊组,术后不同时期观察后囊膜病理变化。结果：术后一月,Ａ组后囊膜纤维增殖明显减少,赤道 后囊膜间无显著粘连,早期即在可在后囊膜面查见纤维弱细胞增生。结论：ＣＣＣ可抑制白内障术后晶体后囊膜混浊的发生。     

化学合成药物抑制单纯疱疹病毒的实验研究

我们使用组织培养技术,对五种化学合成药物抑制单纯庖疹病毒进行了实验研究,现将结果报告如下: 材料和方法1.原代人胚肌皮单层细胞:来自江西省妇女保健院,取孕妇人工流产术后胎儿肌皮组织,用Hanks氏液尽量洗除血球,剪