视网膜色素变性与血管内皮──血小板功能变化

对６５例视网膜色素变性（ＲＰ）患者和３３例正常人进行血浆血栓素Ｂ２（ＴＸＢ２）、６－酮前列腺素Ｆ（１α）（６－Ｋｅｔｏ－ＰＧＦ＿（１α））、血浆丙二醛（ＭＤＡ）、红细胞超氧化物歧化酶（ＳｏＤ），全血谷脱甘肽过氧化物酶活性（ＧＳＨ－ｐＸ）等指标的测定，发现ＲＰ患者血浆ＴＸＢ２以及ＴＸＢ＿２和６－Ｋ－ＰＧＦ１α比值Ｔ／Ｋ均较正常人升高（Ｐ＜０．０５）．６－Ｋ－ＰＧＦ１α和ＳＯＤ较正常人降低（Ｐ＜０．０１）。而ＭＤＡ、ＧＳＨ－ＰＸ无明显改变，表明ＲＰ患者病理过程中存在血管内皮──血小板功能改变以及自由基的损伤。但对ＳＯＤ与ＴＸＢ２、Ｔ／Ｋ比值、６－Ｋ－ＰＧＦ１α的相关分析表明，它们之间无相关性（Ｐ＞０．０５），表明ＲＰ患者虽有血管内皮──血小板功能紊乱，但非自由基损伤所致。     

原发性开角型青光眼房水内皮素与眼压的相关关系研究

目的 了解ＰＯＡＧ房水内皮素与眼压有无相关关系。方法 通过放射免疫饱和分析法（ＲＩＡ）测定高眼压状态的原发性开角型青光眼（ＰＯＡＧ）及正常眼压的白内障患者房水内皮素（ＥＴ）。结果 ＰＯＡＧ组明显高于白内障组（Ｐ〈０．０１）。两组术前眼压比较,Ｐ〈０．０１ＰＯＡＧ眼压和ＥＴ回归分析,Ｐ〈０．０５,白内障组眼压与ＥＴ回归分析,Ｐ〉０．０５。结论 ＰＯＡＧ眼压与ＥＴ分泌有相关关系,眼部ＥＴ水平的改变是机     

原发性开角型青光眼血浆TXA_2－PGI_2测定

为探讨原发性开角型青光眼的发病机理，进行了２９例原发性开角型青光眼病人的血浆ＴＸＡ_２－ＰＧＩ_２的测定，并选择２０例健康人作为对照。测定结果：青光眼组的血浆ＴＸＡ_２均比正常对照组有较显著升高（Ｐ＜０．０１）。说明血浆中的ＴＸＡ_２－ＰＧＩ_２动态平衡失调参与了原发性开角型青光眼的发病机理。     

原发性开角型青光眼血浆TXA2—PGI2测定

为探讨原发性开角型青光眼的发病机理，进行了２９例原发性开角型青光眼病人的血浆ＴＸＡ２－ＰＧＩ２的测定，并选择２０例健康人作为对照，测定结果：青光眼组的血浆ＴＸＡ２的均比正常对照组有较显著升高（Ｐ〈０．０１），说明血浆中的ＴＸＡ２－ＰＧＩ２动态平衡失调参与了原发生开角型青光眼的发病机理。     

BAMBI过表达抑制缺氧诱导的恒河猴视网膜血管内皮细胞增殖和迁移

目的　探讨过表达激活素膜结合抑制剂（ｂｍｐａｎｄａｃｔｉｖｉｎｍｅｍｂｒａｎｅ-ｂｏｕｎｄｉｎｈｉｂｉｔｏｒ,ＢＡＭＢＩ）对缺氧诱导的恒河猴视网膜血管内皮细胞（ＲＦ／６Ａ）增殖和迁移的影响。方法　将ＲＦ／６Ａ细胞分为四组:正常对照组、缺氧组、缺氧＋ｐＦＬＡＧ组和缺氧＋ＢＡＭＢＩ组。Ｗｅｓｔｅｒｎｂｌｏｔ检测各组细胞中ＢＡＭＢＩ的表达,倒置显微镜观察各组细胞形态和密度,ＣＣＫ-８法和流式细胞仪分别检测各组细胞的增殖和周期情况,Ｔｒａｎｓｗｅｌｌ检测细胞的迁移,Ｗｅｓｔｅｒｎｂｌｏｔ检测转化生长因子β１（ｔｒａｎｓｆｏｒｍｉｎｇｇｒｏｗｔｈｆａｃｔｏｒ-β１,ＴＧＦ-β１）和血管内皮生长因子（ｖａｓｃｕｌａｒｅｎｄｏｔｈｅｌｉａｌｇｒｏｗｔｈｆａｃｔｏｒ,ＶＥＧＦ）的表达。结果　与对照组相比,缺氧组细胞数目明显增多,增殖增加,培养１２０ｈ后,对照组细胞增殖倍数为５．００±０．２８,缺氧组为７．６４±０．３２（Ｐ＜０．００１）;缺氧组Ｓ期进程显著加快,占（１０．４４±２．６１）％,对照组Ｓ期占（２０．７９±２．２３）％（Ｐ＜０．０５）;细胞迁移增加,缺氧组细胞数目为３３．８０±４．２０,对照组为８．３５±２．５０（Ｐ＜０．０５）,ＴＧＦ-β１和ＶＥＧＦ的表达明显增加（Ｐ＜０．０５）。缺氧＋ＢＡＭＢＩ组:缺氧处理的细胞转染ｐＦＬＡＧ-ＢＡＭ-ＢＩ后,与缺氧组相比,ＢＡＭＢＩ蛋白表达显著上调,细胞数目明显减少,增殖显著降低,培养１２０ｈ后,增殖倍数为５．５３±０．２７（Ｐ＜０．００１）,细胞Ｓ期受到阻滞,占（１８．７５±２．９２）％,迁移显著下降,数目为１３．００±２．８０（Ｐ＜０．０５）,ＴＧＦ-β１和ＶＥＧＦ的表达明显下调（Ｐ＜０．０５）。结论　过表达ＢＡＭＢＩ可抑制缺氧诱导的ＲＦ／６Ａ细胞的增殖和迁移,进而有望抑制视网膜血管新生。     

胶原性眼内接触镜植入兔眼后前房反应及房水PGE2含量观察

目的：通过兔眼动物实验探讨理想的胶原性眼内接触镜（ＩＣＬ）植入方法。观察ＩＣＬ植入术后炎症反应和炎症介质的变化规律。评定ＩＣＬ眼内植入的生物相容性。方法：将２０只兔子分为三组（植入组、手术组、对照组）,对兔眼ＩＣＬ植入术后不同时间眼压波动,角膜内皮损伤、前房蛋白渗出、前房出血、ＩＣＬ偏位、晶状体混浊等情况进行监测。术后１天、４天、７天、１４天、２８天分别抽取兔眼前房水,采用放射免疫分析测定前列腺素Ｅ２（ＰＧＥ２）浓度。结果：各组手术前后眼压差异无显著意义（Ｐ〉０．０５）。术后出现不同程度角膜内皮混浊、上皮水肿和前房渗出。术后４周均基本消褪。植入组房水中ＰＧＥ２浓度术后１周内明显高于手术组和空白对照组（Ｐ〈０．０５）。以后逐步下降。术后１４天和２８天三组间差异无统计学意义（Ｐ〉０．０５）。结论：ＩＣＬ术后前房反应     

非动脉炎性前部缺血性视神经病变患者血清孕酮水平的变化

目的　观察非动脉炎性前部缺血性视神经病变（ｎｏｎａｒｔｅｒｉｔｉｃａｎｔｅｒｉｏｒｉｓｃｈｅｍｉｃｏｐｔｉｃｎｅｕｒｏｐａｔｈｙ,ＮＡＩＯＮ）患者血清孕酮（ｐｒｏｇｅｓｔｅｒｏｎｅ,ＰＧ）浓度的变化,探讨血清ＰＧ与ＮＡＩＯＮ的关系。方法　将ＮＡＩＯＮ患者４０例作为研究对象,根据病程分为１组（发病１４ｄ内）、２组（＞１４～３０ｄ）、３组（＞３０～６０ｄ）和４组（＞６０～１８０ｄ）;按视盘水肿程度分为重度水肿组、轻度水肿组、水肿消退组。采用化学发光免疫分析法测定ＮＡＩＯＮ患者及年龄相匹配的３０名健康体检者（对照组）的血清ＰＧ水平。统计分析不同性别、病程以及视盘水肿程度的ＮＡＩＯＮ患者与对照组血清ＰＧ水平差异。结果　ＮＡＩＯＮ组较对照组血清ＰＧ水平降低（ｔ＝－４．６８０,Ｐ＜０．０５）。不同性别ＮＡＩＯＮ患者血清ＰＧ水平差异无统计学意义（ｔ＝－０．６４６,Ｐ＞０．０５）。不同病程组间血清ＰＧ水平差异有统计学意义（Ｆ＝１８．９９８,Ｐ＜０．０１）;病程１、２、３组与对照组血清ＰＧ水平比较,差异也均有统计学意义（均为Ｐ＜０．０５）,４组与对照组血清ＰＧ水平比较,差异无统计学意义（Ｐ＞０．０５）。视盘不同水肿程度组间血清ＰＧ水平比较,差异有统计学意义（Ｆ＝１６．７７６,Ｐ＜０．０５）。水肿消退组与对照组血清ＰＧ水平比较,差异无统计学意义（Ｐ＞０．０５）,其余各组间血清ＰＧ水平比较差异均有统计学意义（均为Ｐ＜０．０５）。结论　ＮＡＩＯＮ患者血清ＰＧ水平降低,可能与视盘损害程度相关。     

脉络膜缺血TXB2和6－keto－PGF1a变化及其治疗的实验研究

采用切断兔眼部分睫状后短动脉造成脉络膜缺血的动物模型，测定脉络膜血栓素Ｂ２、（ｔｈｒｏｍｂｏｘａｎｅＢ２，ＴＸＢ２）和６－酮－前列腺素Ｆ１α６－ｋｅｔｏ－ｒｏｓｔａｇｌａｎｄｉｎＦ１α，６－ｋｅｔｏ－ＰＧＦ１α）的含量，并观察复方樟柳碱１号（ｃｏｍｐｏｕｎｄａｎｉｓｏｄｉｎｅＩ，ＣＡＩ）对其影响。结果表明，缺血１ｈＴＸＢ２及６－ｋｅｔｏ－ＰＧＦ１α升高；２４ｈ时６－ｋｅｔｏ－ＰＧＦ１α已呈下降趋势而ＴＸＢ１α仍处于较高水平，使ＴＸＢ２／６－ｋｅｔｏ－ＰＧＦ１α比率升高。ＣＡＩ号升高６－ｋｅｔｏ－ＰＧＦ１α并保持ＴＸＢ２和６－ｋｅｔｏ－ＰＧＦ１α之间的平衡。结果提示，缺血１ｈＴＸＢ２和６－ｋｅｔｏ－ＰＧＦ１α之间的平衡发生变化；ＣＡＩ号改善缺血区脉络膜的微环境并可能调节缺血区血管紧张度。     

紫外光A/核黄素角膜交联后兔角膜基质内基质金属蛋白酶-1含量的变化

目的　检测紫外光Ａ／核黄素角膜交联（ｕｌｔｒａｖｉｏｌｅｔＡ／ｒｉｂｏｆｌａｖｉｎｃｏｒｎｅａｌｃｒｏｓｓ-ｌｉｎｋ-ｉｎｇ,ＵＶＡＲＣＸＬ）后兔角膜基质内基质金属蛋白酶（ｍａｔｒｉｘｍｅｔａｌｌｏｐｒｏｔｅｉｎａｓｅ,ＭＭＰ）-１的短期含量变化。方法　１５只新西兰白兔,随机分为３组,每组５只,Ａ组为空白对照组,Ｂ组为角膜交联后３ｄ,Ｃ组为角膜交联后７ｄ。Ｂ、Ｃ两组行ＵＶＡＲＣＸＬ。各组取角膜后去除角膜上皮和内皮细胞,应用ＥＬＩＳＡ法检测角膜基质内ＭＭＰ-１的含量。结果　Ａ组角膜基质内ＭＭＰ-１／总蛋白含量为（０．１４０±０．０３６）×１０－６,Ｂ组为（０．２４２±０．０５９）×１０－６,Ｃ组为（０．３７２±０．０６１）×１０－６,３组之间差异有统计学意义（Ｆ＝２４．０５１,Ｐ＝０．０００）。ＵＶＡＲＣＸＬ后３ｄ,兔角膜基质内ＭＭＰ-１含量显著升高,与Ａ组相比差异有统计学意义（Ｐ＜０．０５）,术后７ｄ其含量进一步升高,与Ｂ组相比差异有统计学意义（Ｐ＜０．０１）。结论　ＵＶＡＲＣＸＬ后７ｄ内,兔角膜基质内ＭＭＰ-１含量持续增加,推测ＭＭＰ-１可能对ＵＶＡＲＣＸＬ后的角膜基质重塑起一定作用。     

同轴微切口超声乳化白内障吸出术后角膜生物力学变化

目的　比较同轴微切口超声乳化白内障吸出术（ｐｈａｃｏｅｍｕｌｓｉｆｉｃａｔｉｏｎ,Ｐｈａｃｏ）及标准切口Ｐｈａｃｏ术后角膜生物力学的变化。方法　年龄相关性白内障患者３１２例（３１２眼）随机分成两组。其中研究组（２．２ｍｍ同轴微切口组）１５９例,对照组（３．０ｍｍ标准切口组）１５３例。记录两组术前数据,包括年龄、性别、裸眼视力（ｕｎｃｏｒｒｅｃｔｅｄｖｉｓｕａｌａｃｕｉｔｙ,ＵＣ-ＶＡ）、最佳矫正视力（ｂｅｓｔｃｏｒｒｅｃｔｅｄｖｉｓｕａｌａｃｕｉｔｙ,ＢＣＶＡ）、角膜滞后性（ｃｏｒｎｅａｌｈｙｓｔｅｒｅｔｉｅ,ＣＨ）、角膜阻力因数（ｃｏｒｎｅａｌｒｅｓｉｓｔａｎｃｅｆａｃｔｏｒ,ＣＲＦ）、Ｇｏｌｄｍａｎｎ相关眼压（ｇｏｌｄｍａｎｎｃｏｒｒｅｌａｔｅｄｉｎｔｒａｏｃｕｌａｒｐｒｅｓｓｕｒｅ,ＩＯＰｇ）、角膜补偿眼压（ｃｏｒｎｅａｌｃｏｍｐｅｎｓａｔｅｄＩＯＰ,ＩＯＰｃｃ）、中央角膜厚度（ｃｅｎｔｒａｌｃｏｒｎｅａｌｔｈｉｃｋｎｅｓｓ,ＣＣＴ）、角膜内皮细胞计数（ｅｎｄｏｔｈｅｌｉａｌｃｅｌｌｃｏｕｎｔ,ＥＣＣ）;术中数据包括累积能量复合参数（ｃｕｍｕｌａｔｉｖｅｄｉｓｓｉｐａｔｅｄｅｎｅｒｇｙ,ＣＤＥ）、手术时间。术后１ｄ、１周、２周、１个月复查,比较两组ＵＣＶＡ、ＢＣＶＡ、ＥＣＣ、ＣＣＴ、ＣＨ、ＩＯＰｇ、ＣＲＦ和ＩＯＰｃｃ。结果　术后１ｄ两组ＣＨ、ＣＲＦ均较术前明显降低,差异均有统计学意义（均为Ｐ＜０．０５）。术后１周,研究组ＣＨ、ＣＲＦ与术前差异均无统计学意义（均为Ｐ＞０．０５）;对照组ＣＨ、ＣＲＦ较术前降低,差异均有统计学意义（均为Ｐ＜０．０５）。术后２周,两组ＣＨ、ＣＲＦ均恢复至术前水平（均为Ｐ＞０．０５）;两组ＩＯＰｇ、ＩＯＰｃｃ仍高于术前（均为Ｐ＜０．０５）,而低于术后１周（均为Ｐ＜０．０５）;两组ＣＣＴ恢复至术前水平（均为Ｐ＞０．０５）。术后４周,两组ＣＨ、ＣＲＦ、ＩＯＰｇ、ＩＯＰｃｃ、ＣＣＴ均恢复至术前水平（均为Ｐ＞０．０５）。术前,两组ＣＨ、ＣＲＦ与ＣＣＴ存在正相关性（研究组:ｒ１＝０．４３,ｒ２＝０．５２,对照组:ｒ１＝０．５６,ｒ２＝０．５３;均为Ｐ＜０．０５）。术后１ｄ,两组ＣＨ与ＣＣＴ均无相关性（ｒ１＝０．１３,ｒ２＝０．１０,均为Ｐ＞０．０５）。两组的ＣＲＦ值与ＣＣＴ在不同时相始终存在相关性（均为Ｐ＜０．０５）。两组间不同时相的ＣＨ与ＣＲＦ均存在正相关性（均为Ｐ＜０．０５）。结论　同轴微切口Ｐｈａｃｏ和标准切口Ｐｈａｃｏ均会改变角膜生物力学特征。同轴微切口Ｐｈａｃｏ比标准切口Ｐｈａｃｏ术后角膜生物力学特征恢复更快。     

Effect of pilocarpine 4% in combination with latanoprost 0.005% or 8-iso prostaglandin E2 0.1% on intraocular pressure in laser-induced glaucomatous monkey eyes.

PURPOSE: To compare the effect of pilocarpine, an agent that reduces uveoscleral outflow, on the ocular hypotensive efficacy of latanoprost and 8-iso prostaglandin E2 (PGE2). METHODS: Each of the two treatment groups was composed of the same eight monkeys with unilateral laser-induced glaucoma. Intraocular pressure (IOP) was measured hourly for 6 hours beginning at 9:00 AM on the baseline day (Thursday before treatment week) and on treatment days 1, 3, and 5 (Monday, Wednesday, and Friday). On all five treatment days, one drop of pilocarpine 4% was administered at 9:00 AM and 3:00 PM and one drop of latanoprost 0.005% or 25 microL of 8-iso PGE2 0.1% was administered at 10:00 AM and 4:00 PM. RESULTS: One hour after pilocarpine instillation on day 1, the reduction of IOP was similar (P > 0.90) in both treatment groups, 7.6 +/- 1.1 mm Hg (mean +/- standard error of the mean ) in the latanoprost group and 7.4 +/- 0.8 mm Hg in the 8-iso PGE2 group. However, the IOP effects of the two treatment groups became significantly different (P < 0.05) beginning 2 hours after dosing with latanoprost or 8-iso PGE, on day 1. A difference (P < 0.05) between the two groups persisted at all subsequent measurements. The reduction of IOP lessened with repeated dosing in the latanoprost and 8-iso PGE2 groups. Three hours after dosing with pilocarpine and two hours after dosing with the prostanoids, the IOP reduction was 8.3 +/- 0.9 mm Hg in the latanoprost group and 9.9 +/- 0.6 mm Hg in the 8-iso PGE2 group on day 1, and 2.1 +/- 1.0 mm Hg in the latanoprost group and 7.3 +/- 0.9 mm Hg in the 8-iso PGE1 group on day 5. CONCLUSIONS: The smaller reductions in IOP with pilocarpine and latanoprost than with pilocarpine and 8-iso PGE2 show that pilocarpine blocks much more of the ocular hypotensive effect of latanoprost than of 8-iso PGE2. The results also indicate that pilocarpine and latanoprost are mutually antagonistic. Enhancement of uveoscleral outflow appears to account for most of the ocular hypotensive effect of latanoprost and for much less of the ocular hypotensive effect of 8-iso prostaglandin E2.     

Effects of ultraviolet irradiation on prostaglandin-E2 production by cultured corneal stromal cells

We examined the effects of ultraviolet (UV) irradiation on the release of prostaglandin E2 (PGE2) by rabbit corneal stromal cells in culture. Considerable amounts of PGE2 were present in the media of control corneal cultures following 1, 2, 4, 8 and 24 hr of incubation. Irradiation with UV-A (320-400 nm) for 30 min resulted in more than a 50% increase in PGE2 release. Dexamethasone inhibited PGE2 release by corneal stromal cells. It was, however, ineffective in protecting the cells from the UV-induced release of PGE2.     

穿透角膜移植术后房水前列腺素E2及蛋白质量浓度的动态变化

目的　通过对穿透角膜移植术后房水前列腺素E2 (PGE2 )和蛋白质量浓度的测定 ,探讨PGE2 对炎症反应和免疫反应的作用。方法　 42只健康新西兰白兔 ,按穿透角膜移植术的类型和处理方法不同 ,随机分为 6组 ,分别于术后第 10、2 0、3 0、40d抽取各组动物的房水 ,用放射免疫法检测PGE2 质量浓度 ,用紫外分光光度计法测定蛋白质量浓度。结果　自体移植组术后 10d房水PGE2 质量浓度高于对照组 ;同种异体移植组术后 10、2 0d房水PGE2 质量浓度高于对照组 ,1只兔眼于术后 2 0d出现排斥反应 ;异种移植组术后 10、2 0、3 0d房水PGE2 质量浓度均高于对照组 ,有 6只兔眼于观察期内出现明显排斥反应 ;异种移植双氯芬酸钠和地塞米松 (DFNa Dex)治疗组术后 10d房水PGE2 质量浓度低于异种移植Dex治疗组(P <0 0 5 )。房水蛋白质量浓度的变化情况与PGE2 相一致。结论　PGE2 与穿透角膜移植术后的炎症反应和免疫排斥反应密切相关。Dex可抑制异种穿透角膜移植术后的排斥反应。DFNa对Dex有协同作用 ,可减少Dex的用量。     

Effects of topical mydriatics and vasoconstrictors on prostaglandin-E2-induced aqueous flare elevation in pigmented rabbits

We evaluated the effects of topical instillation of mydriatics and vasoconstrictors on prostaglandin E2 (PGE2) induced aqueous flare elevation in pigmented rabbits. Transcorneal diffusion of PGE2 (25 microg/ml) by means of a glass cylinder produced aqueous flare elevation. Mydriatics (atropine sulfate, tropicamide, tropicamide plus phenylephrine hydrochloride, phenylephrine hydrochloride, and cyclopentolate hydrochloride) or vasoconstrictors (naphazoline nitrate and tramazoline hydrochloride) were topically administered before PGE2 application. Aqueous flare was measured with a laser flare-cell meter. One or two instillations of atropine sulfate 1.0%, tropicamide 0.4%, tropicamide 0.5% plus phenylephrine hydrochloride 0.5%, phenylephrine hydrochloride 5.0%, cyclopentrate hydrochloride 1.0%, and naphazoline nitrate 0.05% did not inhibit PGE2-induced aqueous flare elevation. Tramazoline hydrochloride 0.118% inhibited significantly (p < 0.05) PGE2-induced aqueous flare elevation. It is possible that vasoconstriction may be involved partly in inhibition of PGE2-induced aqueous flare elevation by some drugs in pigmented rabbits.     

Effects of topical clonidine on prostaglandin-E(2)-induced aqueous flare elevation in pigmented rabbits

We evaluated the role of topical clonidine on experimental ocular inflammation. Transcorneal diffusion of prostaglandin (PG) E(2), 7. 09 x 10(-2) mmol/l, with the use of a glass cylinder was employed to produce aqueous flare elevation in pigmented rabbits. Clonidine was topically administered and yohimbine was injected intravenously. Aqueous flare was measured with a laser flare cell meter. Topical instillation of 0.25% clonidine inhibited 89% of PGE(2)-induced aqueous flare elevation. Instillation of clonidine at 60 or 30 min before and 10 min after PGE(2) inhibited flare significantly. Pretreatment with intravenous yohimbine decreased the clonidine-induced inhibition of the flare elevation in a dose-dependent manner. It is possible that the anti-inflammatory action of topical clonidine may be mediated partly by alpha(2)-receptors.     

Daily cost of glaucoma medications in China

PURPOSE: To determine and compare the daily cost of various glaucoma medications in China. MATERIALS AND METHODS: The majority of glaucoma medications commercially available in China were included in this research. The total number of drops in 1 bottle of each medication was counted drop by drop. The mean volume per bottle of each medication was calculated. The cost per drop, number of days for both eyes usage per bottle, and daily cost was calculated. RESULTS: (1) The volume per drop ranged from 0.03 mL (brinzolamide 1%, travoprost 0.004%, bimatoprost 0.03%, and latanoprost 0.005%) to 0.05 mL (timolol 0.5%-Chengrui and pilocarpine 0.5% and 2%-Zhenrui). (2) The cost per bottle ranged from $0.69 (US dollar) (timolol 0.5%-Malaisuan Saimaluo'er) to $40.78 (latanoprost 0.005%). (3) The number of days for both eyes usage per bottle ranged from 52 days (bimatoprost 0.03%) to 11 days (pilocarpine nitrate 0.5%-Zhenrui). (4) The daily cost for both eyes usage from expensive to cheap were latanoprost 0.005%-$0.91, travoprost 0.004%-$0.77, brimonidine 0.2%-$0.61, bimatoprost 0.03%-$0.46, D-timolol 1%-$0.36, brinzolamide 1%-$0.34, pilocarpine 2%-Zhenrui-$0.28, levobunolol 0.5%-$0.25, betaxolol 0.25%-$0.24, pilocarpine 0.5%-Zhenrui-$0.18, pilocarpine 2%-Huming-$0.16, carteolol 1%-Mikelan-$0.15, carteolol 2%-Mikelan-$0.15, pilocarpine 1%-Huming-$0.10, timolol 0.5%-Chengrui-$0.08, timolol 0.5%-Malaisuan Saimaluo'er-$0.03. CONCLUSIONS: The daily cost of glaucoma medications in China ranged much more wildly than developed countries. These data may be useful in selecting medications for glaucoma therapy. The ophthalmic solution of prostaglandins is powerful in reducing intraocular pressure. However, its high price should be considered when selecting glaucoma medications in China.     

Effects of topical antiglaucoma eye drops on prostaglandin E(2)-induced aqueous flare elevation in pigmented rabbits

PURPOSE: To evaluate the role of topical instillation of some antiglaucoma agents on experimental elevation of aqueous flare induced by prostaglandin E(2) (PGE(2)) in pigmented rabbits. METHODS: Transcorneal diffusion of PGE(2) (25 microg/mL or 7.09 x 10(-2) mM) with the use of a glass cylinder was achieved to produce aqueous flare elevation in pigmented rabbits. An antiglaucoma agent was topically administered before application of PGE(2). Aqueous flare was measured with a laser flare cell meter. RESULTS: A single instillation of apraclonidine 1.15%, two instillations of epinephrine 1.25%, two instillations of dipivefrin 0.1%, and two instillations and one instillation of dipivefrin 0.04% eye drops inhibited 98%, 96%, 87%, 73%, and 47% of PGE(2)-induced aqueous flare elevation, respectively. Timolol 0.5%, nipradilol 0.25%, dorzolamide 1%, and pilocarpine 2% eye drops had no effects on the increase of PGE(2)-induced flare. CONCLUSIONS: Apraclonidine, epinephrine, and dipivefrin eye drops inhibit PGE(2)-induced elevation of aqueous flare in pigmented rabbits.     

Treatment of diffuse diabetic macular oedema using steroid eye drops

Purpose: To evaluate the efficacy of treatment of diffuse diabetic macular oedema (DME) with difluprednate ophthalmic emulsion 0.05% (Durezol?) in eyes before vitrectomy. Methods: This study enrolled patients with diffuse DME for whom more than 3 months had passed since prior treatment. Nineteen eyes in 15 subjects were treated with difluprednate ophthalmic emulsion 0.05% four times daily for the first month and then twice daily for 2 months (treatment group). As a control group, 22 eyes in 11 subjects with DME were selected from subjects who underwent the steroid responder test. Results: In the treatment group, the mean visual acuity (VA) (±SD) was 0.38 ± 0.25 logMAR and mean retinal thickness was 461.1 ± 109.9 μm at baseline. After 1 month of treatment, the mean VA had improved to 0.29 ± 0.25 (Wilcoxon rank‐sum test, p = 0.30), while mean retinal thickness had decreased to 372.1 ± 70.0 μm (p = 0.006). The rate of effective improvement in retinal thickness was 42% and that of VA was 26%. In the control group, changes in neither VA nor retinal thickness were significant. Conclusions: Eye drop therapy using difluprednate ophthalmic emulsion 0.05% is a useful and effective treatment modality without surgical intervention or severe side‐effects.     

The ocular hypertensive effect of 0.25% fluorometholone in corticosteroid responders

Fourteen subjects known to be corticosteroid responders participated in a double-masked, randomized study comparing the ocular hypertensive effect of 0.25% fluorometholone suspension with that of 0.1% dexamethasone sodium phosphate. Subjects instilled one drop of fluorometholone in one eye and one drop of dexamethasone in the fellow eye four times daily for up to six weeks. Although both medications increased intraocular pressure, endpoint substitution analysis demonstrated that mean intraocular pressure increases from baseline in the eyes treated with fluorometholone were significantly lower than those in the eyes treated with dexamethasone at weeks 2, 4, and 6 (P less than or equal to .05). Also, mean maximum intraocular pressure was significantly lower in the eyes treated with fluorometholone than in the eyes treated with dexamethasone (P = .001). These results indicated that 0.25% fluorometholone is less likely to increase intraocular pressure in corticosteroid responders than 0.1% dexamethasone.     

Comparison of ketorolac 0.4% and bromfenac 0.09% at trough dosing: aqueous drug absorption and prostaglandin E2 levels

PURPOSE: To compare aqueous drug concentrations and prostaglandin E(2) (PGE(2)) levels in patients treated with ketorolac 0.4% and bromfenac 0.09% at trough dosing. SETTING: Private practice, Wilkes-Barre, Pennsylvania, USA. METHODS: This single-center randomized investigator-masked clinical study comprised 56 patients having cataract surgery. Patients received 1 drop of ketorolac 0.4% or bromfenac 0.09% 6 hours and 12 hours preoperatively consistent with on-label dosing schedules. Aqueous humor was collected at the start of surgery and analyzed for concentrations of ketorolac and bromfenac using a reverse-phase high-performance liquid chromatography-mass spectroscopy system and for PGE(2) levels by competitive enzyme immunoassay. RESULTS: The mean aqueous PGE(2) level was 204.2 pg/mL +/- 95.5 (SD) in patients treated with ketorolac 0.4% and 263.7 +/- 90.0 pg/mL in patients treated with bromfenac 0.09%, (P = .020). The mean aqueous concentration of ketorolac and bromfenac at trough dosing was 130.5 +/- 37.8 ng/mL and 6.2 +/- 3.1 ng/mL, respectively (P = .004). CONCLUSIONS: Higher aqueous levels and greater PGE(2) inhibition were observed in cataract surgery patients treated with ketorolac 0.4% than in patients treated with bromfenac 0.09% at trough dosing. These findings suggest that ketorolac 0.4% administered 4 times a day may provide better control of prostaglandin-mediated inflammation than bromfenac 0.09% administered twice a day.