5-Fu抑制兔眼滤过道成纤维细胞的AgNORs表达

目的　应用细胞增殖指标AgNORs,研究兔眼滤过道成纤维细胞 (Fb)增殖规律及 5 Fu的抗增殖作用。方法　取兔眼滤过道切片作AgNORs及HE染色 ,比较 5 Fu眼和对照眼FbAgNORs染色颗粒数量。结果　对照眼滤过道的咬切口、巩膜瓣下、结膜瓣下均有Fb增殖 ,且增殖活性第 7天最高 ,第 3 0天最低。 5 Fu眼FbAgNORs颗粒数显著低于对照眼 ,5 Fu抑制率为 44.9%～ 73 .0 %。结论　 5 Fu可以有效抑制咬切口、巩膜瓣下、结膜瓣下Fb的增殖活性     

MMC对兔眼滤过道成纤维细胞活性的抑制作用

目的：应用细胞增殖指标核仁组成区相关嗜银蛋白（AgNORs),研究兔眼滤过道成纤维细胞（Fb)增殖规律及丝裂霉素C（MMC）的抗增殖作用,并对其临床意义进行探讨。方法：邓兔眼滤过道切片作AgNORs及HE染色,比较MMC眼和对照眼Fb AgNORs染色颗粒数量。结果：不同手术区MMC眼Fb AgNORs颗粒数显著低于对照眼,MMC抑制率为50.7%-82.1%。结论：丝裂毒素C可以有效抑制咬切口、巩膜瓣下、结膜瓣下Fb的增殖活性,抑制作用稍强于同类药物5-Fu。     

羊膜对兔眼滤过道成纤维细胞活性的抑制作用

目的:应用细胞增殖指标核仁组成区相关嗜银蛋白(AgNORs),研究兔眼滤过道成纤维细胞(Fb)增殖规律及羊膜的抗增殖作用,并对其临床意义进行探讨。方法:模仿人眼滤过手术方式行兔眼巩膜瓣下巩膜咬切术,切开前房前巩膜瓣下植入5mm×6mm大小的羊膜,术后1,2,3,4wk取兔眼滤过道标本,作AgNORs及HE染色,比较羊膜眼和对照眼FbAgNORs染色颗粒数量、眼压、滤过泡变化。结果:不同手术区羊膜眼FbAgNORs颗粒数显著低于对照眼,羊膜抑制率为10.8%～59.5%,羊膜眼眼压低于对照眼,术后3,4wk差异有显著性;羊膜眼滤过泡保持时间1～4wk,对照眼为1～2wk。结论:羊膜可以有效抑制滤过道Fb的增殖活性、延长眼压下降和滤过泡保留时间。     

5—Fu抑制兔眼滤过术后成纤维细胞的AgNORs表达

应用细胞增殖指标ＡｇＮＯＲｓ,研究兔眼滤过道成道成纤维细胞增殖规律及５－Ｆｕ的抗增殖作用。方法取兔眼滤过道切片作ＡｇＮＯＲｓ及ＨＥ染色,比较５－Ｆｕ眼和对照眼,ＦｂＡｇＮＯＲｓ染色颗粒数量。结果对照眼滤过道的咬切口,巩膜瓣下,结膜瓣下均有Ｆｂ增殖,且增殖活性第７天最高,第３０天最低。     

蛇毒制剂对兔眼滤过术的影响

目的评价蛇毒制剂在兔眼滤过术后抗瘢痕形成的效果和眼毒性.方法对10只兔双眼行巩膜全层咬切术,术后实验组球结膜下注射5×10-2U/ml的蛇毒制剂0.5ml,对照组注射等量生理盐水,裂隙灯观察眼前段.术后第21天,用鼠尾胶原作为房水外流示踪剂行前房恒压灌注及原位固定,对手术区组织行功能及组织形态学检查.结果术后14,21天,实验组有5眼、3眼可见滤过泡,对照组无1眼有滤过泡.滤过泡消失眼的滤过口被瘢痕组织封闭,手术区结膜下纤维组织明显增生.有滤过泡眼的滤过口仍显开放,房水示踪剂经此开口流入滤过泡.结论蛇毒制剂能抑制兔眼滤过术后结膜下过分瘢痕化,延长滤过泡的存在时间和功能,其眼毒性不明显.     

水分离时应用三氧化二砷抑制兔眼后囊膜混浊及其眼内毒性的实验研究

目的探讨术中水分离时应用三氧化二砷（As2O3）对兔后发性白内障的抑制作用及对兔眼的毒性作用。方法在免眼晶状体囊外摘出术中，应用1mL不同浓度的As2O3（2μmol·L^-1、4μmol·L^-1、8μmol·L^-1）于晶状体囊袋内进行水分离，使其直接短暂作用于晶状体上皮细胞。术后随访12周，裂隙灯观察比较用药组和对照组免晶状体后囊膜混浊、眼压的变化等；并观察术后组织病理学的变化。结果术后2周只有对照组眼出现后囊膜混浊。术后4周用药组眼的后囊膜混浊明显比对照组眼轻，且随药物浓度增高而减轻。中、低浓度组兔眼的术后炎症反应与对照组比较无明显差异。高浓度组兔眼术后早期出现轻微的毒性反应。组织病理学检查表明，对照组的晶状体上皮细胞增生较用药组明显。As2O3可引起晶状体上皮细胞变性，其文化程度与药物浓度有关。高浓度组可引起角膜内皮细胞亚细胞水平可逆性损伤和虹膜睫状体急性炎症反应。结论As2O3能有效的抑制晶状体上皮细胞的增生，其作用强度与药物浓度有关。兔晶状体囊袋内应用2～8μmol·L^-1的As2O3是防治后发性白内障安全有效的荆量浓度。[眼科新进展2007；27（3）：179-183]     

非穿透性小梁切除术联合低浓度丝裂霉素C的实验研究

目的探讨应用低浓度丝裂霉素C的非穿透性小梁切除术后手术区的形态学变化及房水引流途径.方法新西兰白兔12只(24眼),随机分为实验组9只(18眼)和正常对照组3只(6眼).实验组兔双眼行非穿透性小梁切除术,分剐于术后1d、14d、1个月时随机选择3只兔,一眼前房注入辣根过氧化物酶(horseradish pemxidase,HRP),另一眼前房注入相对分子质量为70 000四甲基罗丹明标记的葡聚糖(tetramethyl rhodamine-dextran,TMR-D).60 min后经颈动脉灌注固定,摘取眼球,冰冻切片,观察示踪剂的分布及手术区的形态学变化.正常对照组3只兔,双眼未行手术,示踪剂前房注入方法同前.结果实验组兔眼滤过泡及浅层巩膜瓣下的滤过腔于术后1d及14d时可见HRP强染色.术后14d时,滤过腔内未见明显纤维组织形成,滤过腔周围观膜内有HRP散在染色.术后1个月时,滤过腔局限,少量HRP颗粒分布,滤过腔见纤维组织增生.正常对照组结膜下仅微弱HRP显色,巩膜内无HRP颗粒分布.实验组及正常对照组脉络膜均可见TMR-D红色荧光.结论非穿透性小梁切除术后房水引流途径涉及结膜下外滤过、巩膜内吸收及葡萄膜巩膜引流.     

Avastin抑制兔眼小梁切除术后滤过泡瘢痕化的作用

目的:探讨Avastin抑制兔眼小梁切除术后滤过泡纤维瘢痕形成的作用。方法:兔20只40眼随机分为3个不同剂量Avastin实验组、丝裂霉素C(MMC)对照组及空白对照组。对兔眼行常规小梁切除术,Avastin实验组于术毕及术后3,7d术区结膜下分别注射0.5,1及2mg Avastin;MMC对照组术中筋膜囊、巩膜瓣下放置0.2g/LMMC棉片。术后裂隙灯下观察滤过泡形态及角膜、前房等情况;术后7,14d摘除眼球,常规HE染色观察组织形态,在高倍视野中,通过滤过泡腔面在结膜中形成的面积百分比及滤过泡形成区在结膜中面积百分比,评价不同剂量Avastin结膜下注射对滤过泡形成及纤维化的影响。结果:术后7d各组结膜纤维结缔组织中均可见明显的滤过泡形成。术后14d仅注射2mg Avastin实验组及MMC对照组的结膜组织中可见明显滤过泡;1mg Avastin实验组见少量面积微小的滤过泡;0.5mg Avastin实验组及空白对照组滤过泡均消失,纤维组织增生明显。术后7d各组高倍视野下滤过泡腔面在结膜中形成的面积百分比及滤过泡形成区在结膜中面积百分比无明显差异。术后14d,2mg及1mg Avastin实验组滤过泡腔面积在结膜中形成的面积百分比分别为1.0%,0.8%,MMC组为0.9%。2mg及1mgAvastin实验组滤过泡形成区在结膜中面积百分比分别为26.1%,2.9%,MMC组为25.8%。2mg及1mgAvastin实验组的滤过泡腔面及形成区面积与结膜面积的百分比均明显高于空白对照组,单项方差分析结果分别为F=270.10,P=0.00;F=49.99,P=0.00;2mg Avastin实验组的上述滤过泡面积百分比与MMC组无差异。结论:结膜下注射Avastin可有效帮助滤过术后滤过泡的形成与维持,缓解滤过泡的纤维增生。     

高三尖杉酯碱脂质体及高三尖杉酯碱 注射液对兔滤过术的作用

目的研究高三尖杉酯碱（ｈｏｍｏｈａｒｉｎｇｔｏｎｉｎｅ,ＨＨＴ）脂质体及高三尖杉酯碱注射液对兔滤过术后抗瘢痕形成的疗效及毒性。方法对４０只家兔双眼行巩膜后唇咬切术,自术后次日起,第１组结膜下注射ＨＨＴ脂质体,第２组结膜下注射空白脂质体（对照组）,第３组结膜下注射低剂量ＨＨＴ注射液,第４组结膜下注射生理盐水（对照组）,第５组结膜下注射高剂量ＨＨＴ注射液。结果２个对照组的滤过泡在术后７天失败,低剂量ＨＨＴ组的滤过泡在术后９天失败,ＨＨＴ脂质体组的滤过泡在术后１２天失败,高剂量ＨＨＴ组的滤过泡在术后１５天失败。术后５～１０天,高剂量ＨＨＴ组的巩膜瘘道阻塞率为３７５％,其余４组的阻塞率均为１０００％;术后１５～３０天,５组的巩膜瘘道阻塞率均为１０００％。高剂量ＨＨＴ组中６３０％的眼出现中至重度角膜水肿及角膜血管翳。结论对兔眼滤过术后应用ＨＨＴ脂质体和低剂量ＨＨＴ注射液不能明显提高兔眼滤过术的成功率。应用高剂量ＨＨＴ注射液可暂时提高兔眼滤过术的成功率,但副作用亦明显增加。     

可降解聚合微球持续释放5-氟脲嘧啶作为滤过手术的辅助治疗

目的:研究 5 Fu高分子微球对实验性质滤过术后瘢痕形成的疗效及毒性。方法 :对 40只兔行巩膜后唇咬切术 ,实验组术中结膜下注射 1ml 5 Fu微球 ,对照组术中结膜下注射 2 5 % 5 Fu注射液 10mg。结果 :术后实验组和对照组眼内压和滤过泡的存留有显著性差异。 5 Fu微球药物浓度变化范围 2 6 47～ 9 872ug/ml,持续 14天 ,可降低它的毒性 ,组织学显示两组纤维增生有显著差异。结论 :PTL EO PLA聚合微球通过释放 5 Fu ,防止瘢痕增殖引起的滤过不畅 ,降低 5 Fu的毒性 ,提高兔眼滤过术的成功率 ,有临床应用价值     

Strabisme Alternant - Etude clinique - traitement

The author defines motor and sensory alternation: the term alternation should not be used in isolation, it should always be accompanied by the name of the parameter concerned. Sensory alternation is always found together with motor alternation but the reverse is not true.The examining criteria for a diagnosis of sensory alternation are given, sensory alternation must not be confused with alternating inhibition. Working from clinical observations of cases of motor alternating strabismus, the author selects 2 types of binocular sensory relations which allow one to differentiate between:- cases of primary alternating strabismus- cases of secondary alternating strabismusThese forms will develop in different ways; in both cases a cure is possible providing that the right treatment is prescribed and once prescribed carefully followed, etc. It is always a case of serious forms of strabismus whose developmental period is spread over several years.According to the authors, the frequency of cases of true primary strabismus is from 1–3%, the frequency of cases of secondary alternating strabismus varies according to the type of therapy practised on cases of monocular strabismus with amblyopia. These latter will become cases of alternating strabismus under the influence of certain types of therapy carried out over several years (penalization, rocking, alternated occlusion, etc...).Experimental data on kittens confirm clinical data; kittens placed in abnormal environments during the sensitive period will show modification in the distribution of cortical cells and the absence of binocular cells (either because the excitation of the two eyes was not simultaneous, or not identical: artificial strabismus, occlusion, opaque glasses). This disturbances become irreversible after a certain period of exposure (a function of age, length of exposure, etc...).It is thus necessary to bear in mind: 1) the iatrogenic risks of certain orthoptic treatments, 2) the necessity for a binocular form of treatment as soon as possible, as once a certain stage is passed, cortical plasticity diminishes and the elaboration of normal binocular relations becomes impossible.

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Effects of Adenosine Agonists on Intraocular Pressure and Aqueous Humor Dynamics in Cynomolgus Monkeys

The effects of single or multiple topical doses of the relatively selective A₁adenosine receptor agonists (R)-phenylisopropyladenosine (R-PIA) and N⁶-cyclohexyladenosine (CHA) on intraocular pressure (IOP), aqueous humor flow (AHF) and outflow facility were investigated in ocular normotensive cynomolgus monkeys. IOP and AHF were determined, under ketamine anesthesia, by Goldmann applanation tonometry and fluorophotometry, respectively. Total outflow facility was determined by anterior chamber perfusion under pentobarbital anesthesia. A single unilateral topical application of R-PIA (20–250 μg) or CHA (20–500 μg) produced ocular hypertension (maximum rise=4.9 or 3.5 mmHg) within 30 min, followed by ocular hypotension (maximum fall=2.1 or 3.6 mmHg) from 2–6 hr. The relatively selective adenosine A₂antagonist 3,7-dimethyl-1-propargylxanthine (DMPX, 320 μg) inhibited the early hypertension, without influencing the hypotension. Neither 100 μg R-PIA nor 500 μg CHA clearly altered AHF. Total outflow facility was increased by 71% 3 hr after 100 μg R-PIA. In conclusion, the early ocular hypertension produced by topical adenosine agonists in cynomolgus monkeys is associated with the activation of adenosine A₂receptors, while the subsequent hypotension appears to be mediated by adenosine A₁receptors and results primarily from increased outflow facility.