急性闭角型青光眼持续高眼压下的手术治疗

目的探讨急性闭角型青光眼发作期持续高眼压状态下手术的特点及效果。方法对应用大剂量降眼压药物2~3天后眼压仍持续在40mmHg以上的60例65眼施行小梁切除术。术中先间断地缓慢放出房水,减低眼压后进行小梁切除术。术后随访6个月。结果65眼术前视力均在0.05以下。术后1周视力≥0.05者64眼,视力≥0.3者31眼;眼压≤21mmHg者52眼。术中术后无玻璃体脱出、脉络膜脱离、脉络膜下大出血或睫状环阻塞性青光眼等并发症发生。结论急性闭角型青光眼持续高眼压时,小梁切除术术中多次间断缓慢放出房水对持续高眼压状态下的治疗是安全有效的。     

高眼压状态下青光眼小梁切除术的临床分析

目的：探讨青光眼高眼压状态下小梁切除术的安全性和有效性。

方法：对25例26眼充分降眼压后眼压仍不正常的青光眼患者, 前房穿刺放出房水后行复合小梁切除术,观察疗效及术后并发症。

结果：所有手术均顺利完成, 未出现暴发性脉络膜出血、玻璃体脱出等严重并发症,术后眼压控制≤21mmHg,术后视力提高25眼,总有效率96.2%。

结论：小梁切除术治疗青光眼安全、简便、可靠。对药物不能控制的持续性高眼压状态下的青光眼,放出房水后再行复合小梁切除术仍是最有效的理想术式。     

高眼压状态下急性闭角型青光眼的手术方法和效果

目的 探讨持续高眼压状态下急性闭角型青光眼的方法和临床效果.方法 42例( 45眼)急性闭角型青光眼在高眼压状态下行小梁切除术,术前及术中两次穿刺缓慢放出房水;术后相和拆除可调节缝线、眼球按摩及滤过泡分离手术等处理.随访观察滤过泡、前房、眼压、视力及并发症.结果 42例(45眼)手术顺利,无脉络膜下爆发性出血或玻璃体脱出等严重并发症.结论 急性闭角型青光眼在高眼压状态下行小梁切除术,只要手术前后处理得当,是安全有效的.     

高眼压下急性闭角型青光眼小梁切除术的临床观察

目的探讨急性闭角型青光眼发作期持续高眼压状态下行小梁切除术的可行性及效果。方法对应用大剂量降眼压药物2~3 d后眼压仍持续在40 mmHg以上的40例(65眼)行小梁切除术;术中均在切除小梁组织前在巩膜瓣根部中央角膜缘处用剃须刀刺开一小切口,缓慢放出房水,眼压降低后再常规完成手术。结果本组术中及术后均未出现暴发性脉络膜上腔出血、恶性青光眼等严重并发症,术后1周视力≥0.1者64眼;视力≥0.3者39眼;眼压≤21 mmHg者52眼;术后3眼出现脉络膜脱离,7眼前房形成延缓,经治疗后逐渐恢复。本组病例手术后大多数保留了较好的视力。结论药物不能控制眼压的急性闭角型青光眼,及时行前房穿刺加小梁切除术手术治疗十分必要,可以避免视功能的进一步损害。     

急性高眼压下猫眼视网膜酶的活性改变

我们用酶组化方法系统观察急性高眼压下猫眼视网膜及其血管１０种酶活性的改变，这些改变亦即视网膜缺血－再灌流所引起的损害，自由基清除剂过氧化氢酶和过氧化物酶活性降低，证明自由基增多是造成上述损害的之一，其处理原则为在降低高眼压的同时，缺血期宜通过血循环以外途径补充视网膜所急需的氧和营养物，缺血后的再灌流期给予自由基清除剂。     

持续高眼压状态下青光眼手术探讨

目的：探讨持续高眼压青光眼的手术治疗的注意事项。方法：对55例61眼高眼压青光眼用各种药物降低眼压后，进行巩膜下咬切＋虹膜周边或全切，小梁切除术，青光眼滤过手术＋白内障囊外摘出术。术前尽量降低眼压，减轻葡萄膜反应；术中减少对组织的损伤，切开前房时，缓慢放出房水；术后密切观察前房深度、葡萄膜反应及眼压，及时对症处理。结果：术后1月眼压＜20mmHg占85％，21-25mmHg4眼，26－30mmHg5眼（1mmHg=0.133kPa）；视力提高者32眼，占52％，无变化13眼，下降16眼。结论：持续高眼压状态下青光眼手术可以挽救大部分患者的视功能，但须在术前、术中及术后采取缜密措施。     

前房穿刺在青光眼治疗中的应用

目的:探讨前房穿刺术在青光眼治疗中的临床应用。方法:对210例239眼青光眼患者在术前或术中实施前房穿刺以降低眼压或观察手术效果等。其中22眼为急性闭角型青光眼急性发作高眼压经药物治疗不能有效控制的患者,行前房穿刺放出房水降低眼压;217眼为青光眼小梁切除术中常规行前房穿刺放出房水,注入平衡盐,以调节眼压,促进前房及滤枕形成,预防并发症发生。结果:急性高眼压患者经前房穿刺放液后症状迅速缓解,眼压下降,视力提高;青光眼做小梁切除术后除5例5眼发生Ⅰ度浅前房外,未见其它并发症。结论:前房穿刺应用于青光眼治疗中是降低眼压、预防术中及术后并发症的有效方法,特别适合于基层医院推广。     

银杏叶黄酮对兔实验性高眼压后视网膜组织氢氧根自由基的影响

观察银杏叶黄酮对实验性兔高眼压视网膜组织氢氧根(OH)自由基的影响。 方法 用前房灌注生理盐水法制成急性高眼压模型后,治疗组静脉注射不同剂量的银杏叶黄酮,对照组静脉注射生理盐水,70 h后所有组静脉注射水杨酸钠,以2.3-二羟安息香酸(2.3-DHBA)形式捕捉OH,用高效液相色谱仪结合电化学荧光仪检测2.3-DHBA的含量,用电化学荧光仪检测水杨酸盐的含量,来分析兔视网膜组织巾的自由基的含量。结果 经过5 h的高眼压后眼压恢复到15 mmHg,72 h后,模型组兔视网膜组织中的自由基的水平比对照组显著增高(P<0.01),银杏叶黄酬治疗后大、中剂量治疗组兔视刚膜组织中的自由基的水平比模型组显著下降(P<0.01),与对照组相比轻度增高但无明显差别。 结论 银杏叶黄酮可清除高眼压状态下视网膜组织中产生的自由基的损害,对高眼压状态下视网膜组织具有重要的保护作用。     

急性高眼压视网膜的自由基损伤及自由基清除剂的应用

本文用家兔急性高眼压模型测定了急性高眼压后不同时期视网膜的ＳＯＤ、ＣＡＹ活性和ＭＤＡ含量，并用ＥＳＲ测定了急性高眼压视膜自由基的波谱，同时用透射电镜观察了急性高眼压后不同时期及应用自由基清除剂ＶｉｔＥ，ＶｉｔＣ后视网膜的超微结构变化，发现急笥高眼压后ＳＯＤ，ＣＡＴ活性降低，而ＭＤＡ含量增高，ＥＳＲ波谱ｇ值２．００１６５，为氧自由基。超微结构显示视细胞盘膜扭曲，内段线粒体膨胀。应用自由基清除剂Ｖｉｔ     

改良式小梁切除术在持续高眼压的青光眼手术中的应用

目的 观察持续高眼压状态下青光眼手术中改良式小梁切除术的临床应用效果。方法将改良式小梁切除术应用于持续高眼压状态下的急性闭角型青光眼的治疗,共52例（65眼）。采用表面麻醉和2％利多卡因棉片浸润麻醉。用隧道刀做板层巩膜瓣;在小梁切除部位做前房穿刺,慢放房水;术中散瞳,术毕睫状肌麻痹剂应用。结果术中术后均未出现脉络膜出血、脉络膜脱离、玻璃体脱出或睫状环阻塞性青光眼等严重并发症。随访3—6个月,眼压控制正常,视力无下降。结论改良小梁切除术应用于持续高眼压状态下青光眼安全有效,及时手术能维持部分视功能。     

Glutathione and ocular photobiology

Glutathione is present in both the reduced and oxidized form in the cornea, aqueous humor, ocular lens and retina. In these tissues it serves a variety of functions including maintaining normal tissue hydration (in the cornea) detoxifying peroxides and electrophilic compounds via enzymatic pathways and acting as a free radical scavenger to protect against photoinduced damage. In the ocular lens, glutathione levels decrease with aging and cataract formation. Recent evidence which may account in part for this phenomenon suggests that glutathione is altered when subjected to UV radiation in the presence of H2O2. Analyses employing fluorescence, phosphorescence, UV absorption and proton mode NMR spectroscopy demonstrate that UV exposure does alter both the reduced and oxidized forms of glutathione, producing the same final products. Moreover, while H2O2 speeds up the process, it is not essential to the reaction.     

Superoxide dismutase and catalase of calf trabecular meshwork

Superoxide dismutase and catalase activities have been measured in cell-free extracts of calf trabecular meshwork, and for comparison, in calf iris, retina, lens, liver, and erythrocytes. Gel electrophoresis has been used to identify isozymes of each enzyme. The superoxide dismutase and catalase activities per milligram wet weight of calf trabecular meshwork, 0.184 and 0.884 U/mg wet wt, respectively, were comparable to those found in iris and retina, and much higher than those found in lens. Three isozymes of superoxide dismutase were identified in trabecular meshwork. Two of these presumably correspond to cytoplasmic superoxide dismutase, while the third corresponds to a mitochondrial isozyme. A presumably mitochondrial superoxide dismutase activity was also observed in iris and retina, but not in lens. A single catalase isozyme was found in all tissues examined. At physiologic H2O2 concentrations, catalase may have similar levels of activity to glutathione peroxidase. Superoxide dismutase, catalase, and glutathione peroxidase may constitute an important defense mechanism of trabecular meshwork against the toxic O2-. and H2O2 to which it must be continuously exposed from endogenous production as well as from the aqueous humor.     

Myocilin-associated exosomes in human ocular samples

Mutations in myocilin result in ocular hypertension, likely due to decreased drainage of aqueous humor through the trabecular meshwork. Since less myocilin is found in the aqueous humor of those with disease-causing mutations, understanding myocilin's role in the aqueous humor is of clinical importance. Recently, myocilin was shown to exit cultured trabecular meshwork cells in association with shed vesicles called exosomes. To examine relevance of this finding in a physiological setting, the present study examined three different types of ocular samples for the presence of myocilin-associated exosomes. Using differential centrifugation steps, we found myocilin associated with exosomes isolated from effluent collected from human anterior segments in organ culture and aqueous humor obtained from human cadaveric eyes or from patients undergoing excisional surgery. Similar to results with cultured cells, myocilin associated predominately with exosomes in fresh samples, appeared mostly soluble at later times, and had biochemical properties (density of 1.13-1.19 g/ml in linear sucrose gradient) similar to those characteristics of exosomes. These data indicate that exosomes are present and may facilitate the transport of myocilin into the extracellular space of human ocular cells.     

用高效液相法行人眼组织氨基酸含量测定

目的 探讨用高效液相（HPLC）PICO－TAG分析法测定正常成年人眼内玻璃体、晶状体、视网膜和色素膜内17种游离和水解氨基酸含量。方法 将以上组织标本依不同要求分别制成游离或水解组织标本，采用A，B双泵梯度法洗脱，以RonVERSION3．86软件系统对各峰面积分析。结果 该方法对晶状体、视网膜和色素膜各组织内水解氨基酸的分离效果均很好，对玻璃体不论是水解还是游离样本，除对缬氨酸、蛋氨酸和胱氨酸无法将这3种氨基酸分离开，对其他氨基酸的分离效果均不错。结论 首次对我国正常成年人眼内组织17种游离和水解氨基酸做了测定，并提供了一种HPLC眼组织游离和水解氨基酸样本的制备方法。     

Localization of nitric oxide synthase isoforms in porcine ocular tissues.

PURPOSE: To determine by immunohistochemistry the distribution of different nitric oxide synthases (NOS) isoforms in the porcine eye. METHODS: By light microscopy (immunofluorescence), porcine ocular tissues were investigated using monoclonal antibodies against neuronal NOS (nNOS; NOS I), endothelial NOS (ecNOS; NOS III), and macrophage NOS (macNOS; NOS II). RESULTS: Specific nNOS immunoreactivity was detected along the apical cytoplasmic portions of the non-pigmented and pigmented ciliary epithelial cells, in the endothelial lining of the corneoscleral meshwork and the uveal cords of the iridocorneal angle tissue, as well as in the photoreceptor layer of the sensory retina. Immunoreactivity for ecNOS was confined to the vascular endothelium of the vessels of the conjunctiva, iris, ciliary body, retina, choroid and optic nerve. A mild immunostaining for macNOS was present in the cytoplasm of some non-pigmented ciliary epithelial cells. CONCLUSIONS: The predominant localization of nNOS in ciliary epithelial and trabecular endothelial cells suggests a possible involvement of nNOS in both the production and outflow of aqueous humor in porcine eyes.     

Therapy with 9-beta-D-arabinofuranosyladenine (ARA-A) and 2'-deoxycoformycin increases the ARA-A content of ocular tissues

The amount of 9-beta-D-arabinofuranosyladenine (ARA-A) and 9-beta-D-arabinofuranosylhypoxanthine (ARA-Hx) present in ocular tissues of rabbits was determined following therapy with ARA-A alone and when ARA-A was used in combination with 2'-deoxycoformycin (dCF). Topical therapy was initiated three days after infection of the corneas of rabbits with herpes simplex virus type 1. Ocular tissues were harvested after two days of therapy and analyzed by high performance liquid chromatography. Combination topical therapy with ARA-A and dCF significantly increased the tissue content of ARA-A in all tissues examined except retina, as compared to therapy with ARA-A alone. The ARA-A content of the two ocular tissues most often subject to acute herpes infections, the conjunctiva and cornea, was increased from 29.9 +/- 11.7 to 144.0 +/- 53.3 pmoles/mg dry weight and from 15.4 +/- 6.1 to 231.8 +/- 30.8 pmoles/mg dry weight, respectively. Except for the aqueous humor, the total arabinoside content of each tissue was not significantly altered by combination therapy, merely the ratio of ARA-A to ARA-Hx was changed. These studies demonstrate that combination topical therapy with ARA-A and an inhibitor of ARA-A catabolism, dCF, can effectively result in elevated amounts of ARA-A in ocular tissues.     

Distribution of glucocorticoid and mineralocorticoid receptors and 11beta-hydroxysteroid dehydrogenases in human and rat ocular tissues

PURPOSE: The administration of glucocorticoids as topical or systemic medications may lead to the development of ocular hypertension through the induction of morphologic and biochemical changes in the trabecular meshwork leading to a reduction in the facility of aqueous outflow. Glucocorticoids exert their physiological effects by binding to and activating glucocorticoid and mineralocorticoid receptors. The activity of glucocorticoids is critically regulated at a prereceptor level by the two isozymes of 11beta-hydroxysteroid dehydrogenase. The purpose of this study was to determine the distribution of glucocorticoid target receptors and the isozymes of 11beta-hydroxysteroid dehydrogenase (11 beta-HSD) that regulate the activity of glucocorticoids at a prereceptor level in human and rat ocular tissues. METHODS: Horizontal sections of normal adult human and rat eyes were cut and hybridized with 35S-labeled cRNA probes specific for the glucocorticoid receptor, mineralocorticoid receptor, and 11beta-HSD types 1 and 2 using in situ hybridization. Immunohistochemical analysis of glucocorticoid and mineralocorticoid receptors using monoclonal antibodies was carried out on rat eye tissue sections. Whole rat eyes were homogenized and the activity of 11beta-HSD types 1 and 2 in the eye assessed as the percentage conversion of tritiated corticosterone to tritiated 11-dehydrocortico-sterone when corticosterone was added to the homogenate. RESULTS: In the rat ocular tissues mRNAs encoding glucocorticoid receptor, mineralocorticoid receptor, and 11beta-HSD types 1 and 2 were detected in nonpigmented ciliary epithelium, trabecular meshwork, corneal epithelium and endothelium, and anterior lens epithelium. Immunohistochemistry confirmed the presence of glucocorticoid and mineralocorticoid receptors at these sites. Activity of both isozymes of 11beta-HSD was demonstrated in homogenized rat eyes (percentage conversion of tritiated corticosterone to 11-dehydrocorticosterone; mean +/- SD, 11beta-HSD 1 = 15% +/- 5.3%, 11beta-HSD 2 = 7.9% +/- 2.8%). In both human and rat eyes, expression of mRNAs encoding glucocorticoid receptor and 11beta-HSD type 1 was high in the trabecular meshwork and lens epithelium, whereas expression of mRNAs encoding the mineralocorticoid receptor and 11beta-HSD type 2 was high in nonpigmented ciliary epithelium and corneal epithelium and endothelium. CONCLUSIONS: Glucocorticoid target receptors and the enzymes regulating glucocorticoid activity at these receptors are present in mammalian ocular tissues, which regulate aqueous humor formation and outflow. Alteration in the number or affinity of receptors or in the activity of regulatory enzymes may alter the susceptibility of certain individuals to the effects of glucocorticoids on intraocular pressure.     

原花青素对大鼠急性高眼压后视网膜作用的实验研究

探讨原花青素(PC)对大鼠急性高眼压后视网膜的作用及其机制。方法 将Spraque-Dawley(SD)大鼠随机分成正常组、模型组及PC高、低剂量组。PC高、低剂量组用原花青素蒸馏水悬浊液分别按100 mg/（kg·d）和300 mg/（kg·d）灌胃给药5 d,正常对照组和模型组则同步灌注蒸馏水,5d后模型组和PC各剂量组分别建立急性高眼压模型,48 h后取出建立高眼压模型的眼球。电子显微镜观察各组视网膜形态结构,紫外分光光度计比色法检测视网膜组织匀浆中超氧化物歧化酶（SOD）、丙二醛 （MDA）、一氧化氮（NO）、谷氨酸（Glu）和钙离子（Ca2+）水平。结果 电子显微镜图片显示PC可减轻视网膜组织水肿,减少视网膜神经节细胞凋亡。PC可提高视网膜组织中SOD活性,降低MDA、NO、Glu和Ca2+水平。结论 PC对急性高眼压导致的视网膜损伤有保护作用,其主要机制可能与抗自由基氧化,拮抗钙离子超载,降低NO及Glu对视网膜的毒性作用有关。     

Aqueous humor dynamics in alpha-chymotrypsin-induced ocular hypertensive rabbits.

Aqueous humor dynamics were studied in alpha-chymotrypsin-induced ocular hypertensive rabbits either by tonographic or two-level constant pressure perfusion techniques. A significant correlation was obtained between the values of outflow facility in alpha-chymotrypsin-induced ocular hypertensive rabbits as determined by tonography and constant pressure perfusion. The mean value of tonographic outflow facility in ocular hypertensive rabbits was not statistically different from that found in ocular normotensive rabbits. On the contrary, the estimated rate of aqueous inflow in ocular hypertensive rabbits was about 1.5-fold higher than that of ocular normotensive ones. While topical timolol lowered intraocular pressure and aqueous humor inflow in ocular hypertensive rabbits, pilocarpine did not produce any significant effect. Aqueous humor protein was significantly increased in ocular hypertensive eyes. The results of this study show that accurate measurements of outflow facility can be obtained in alpha-chymotrypsin-induced ocular hypertensive rabbits by tonographic technique. Our data suggest that the long-term ocular hypertension induced by alpha-chymotrypsin in albino rabbits may be secondary to an increase in the rate of aqueous humor inflow, likely produced by a breakdown of the blood-aqueous barrier. This finding strongly conflicts with the hypothesis of trabecular blockage as the cause of alpha-chymotrypsin-induced ocular hypertension in this species.     

Ascorbic acid inhibits the activity of polymorphonuclear leukocytes in inflamed ocular tissues

Myeloperoxidase (MPO) is present at high levels in polymorphonuclear leukocytes (PMNs) and has been used as a marker to quantify the accumulation of PMNs in inflamed tissues. MPO activity in inflamed ocular tissues was inhibited by aspirates of aqueous humor. This inhibition could be duplicated by the addition of ascorbic acid at concentrations equivalent to those present in the aliquots of aqueous humor. Similarly, aqueous humor and ascorbic acid inhibited MPO from isolated rabbit leukocytes. Therefore, ascorbic acid appears to inhibit the functional activity of the peroxidase in PMNs, thus preventing potential tissue damage by this enzyme when released during leukocyte degranulation in inflammation. Ascorbic acid might fulfill a role as an endogenous anti-inflammatory agent in the eye.