慢性高眼压条件下兔眼视盘及神经纤维层的改变

目的探讨慢性持续性高眼压条件下，兔眼视盘结构和神经纤维层的异常变化。方法12只新西兰白兔随机分为对照组和高眼压组；高眼压组兔眼前房注入0．3％复方卡波姆溶液制作成慢性高眼压模型，对照组仅作前房穿刺。1、2、3、4周时用海德堡视网膜断层扫描仪(Heidelberg retinal tomography，HRT)测量兔眼的视盘面积、盘沿面积、神经纤维层(retinal nerve fiber layer，RNFL)厚度。结果对照眼和模型眼间各参数差异有非常显著性(P值分别为0．001，0．000，0．1300)，沿盘面积和神经纤维层厚度随高眼压持续时间的延长有进行性降低的趋势(P值分别0．001、0．000)。结论HRT可以较早期、准确、动态的检测慢性高眼压视乳头和神经纤维层的变化。     

高眼压猴视盘和视网膜神经节细胞复合体的纵向变化

目的　观察高眼压前后视盘和视网膜神经节细胞复合体（ganglion cell complex,GCC）的纵向变化,探讨高眼压对视盘和GCC的影响。方法　选取实验用恒河猴3只,全部为雄性,年龄4岁,保持在12 h暗和12 h光照（100 Lux）环境中给予水果、蔬菜等混合喂养。3只猴右眼用激光诱发高眼压。检测光凝前后的实验猴眼压,行眼底像和光学相干断层扫描检查。记录基线和3次随访的视盘外观、视网膜神经纤维层（retinal nerve fiber layer,RNFL）的厚度和GCC,对实验结果进行统计学分析。结果　首次光凝后激光眼即刻眼压为（3.00±0.58）mmHg（1 kPa=7.5 mmHg）,明显低于光凝前的眼压（17.33±1.20）mmHg和对侧眼的眼压（17.00±1.53）mmHg,差异均有统计学意义（t=16.25,P=0.004;t=9.17,P=0.010）。首次光凝后近2 a激光眼的眼压为（41.00±5.00）mmHg仍维持在高于光凝前的基线水平,差异有统计学意义（t=6.17,P=0.030）。光凝后4个月时激光眼视盘的颜色开始变淡,8个月时颜色较光凝前明显变淡,12个月时颜色仍然变淡。对侧眼视盘的颜色在光凝后4~12个月都呈现粉红色,与光凝前对比无明显变化。光凝后4个月、8个月和12个月激光眼视盘周围的RNFL厚度都较对侧眼以及光凝前变薄。对侧眼视盘周围的RNFL厚度在光凝后4个月、8个月和12个月与光凝前相比均无明显改变。光凝后4个月、8个月和12个月激光眼黄斑区GCC的厚度与光凝前和对侧眼相比变薄。光凝后4个月、8个月和12个月对侧眼黄斑区GCC的厚度与光凝前相比均无明显改变。结论　在高眼压造成青光眼性视神经病变和视网膜病变之前,视盘和GCC一直处于高眼压和低眼压的波动状态;由此引起的缺血再灌注交替性损伤可能是激光诱导的高眼压模型猴的病理生理特征之一。     

视盘出血对高眼压症转归的临床意义分析

目的 探讨高眼压症中容易进展为青光眼的临床特点,为早期确诊这类青光眼提供帮助.方法 回顾性分析自2002年1月至2007年3月门诊随访的有完整资料的312例高眼压症病人中,发生视盘出血和未发生视盘出血两组病例中进展为青光眼的情况.结果 312例病人中,42例(13.46%)发生视盘出血,其中12例(28.57%)确诊为青光服,无视盘出血的270例(86.54%)病人中33例(12.22%)确诊为青光眼,两组之间差异显著有统计学意义(Pearson chi2=7.8711,Pr=0.005).对各组间眼压进行比较,确诊为青光眼的视盘出血组和视盘未出血组间差异有统计学意义(t=-2.2911,P=0.0269),而视盘出血两组间、视盘未出血两组间和未确诊为青光眼的视盘出血组和视盘未出血组间差异无统计学意义(t=1.8493,P=0.0718;t=0.5915,P=0.5547;t=0.7039,P=0.4821).结论 视盘出血是高眼压症进展为青光眼的一个危险因素,视盘出血且眼压偏高者更容易进展为青光眼.     

光相干断层扫描连续监测大鼠慢性高眼压模型视盘神经纤维厚度变化

目的:用光相干断层扫描（OCT）连续观测大鼠慢性高眼压模型视 盘神经纤维层（RNFL）厚度的变化。 方法:选用Wistar大鼠48只，随机分为3组，每组16只鼠32只眼 ，右眼为激光光凝眼，左眼为对照眼。用波长为532 nm氩激光在全麻下光凝右眼小梁网，引 起眼压 慢性、中等程度升高并观测眼压变化。眼压升高后第3、6、9周时用OCT做视盘线性扫描， 计算机自动测量视盘RNFL厚度，然后处死大鼠，将每组8只大鼠右眼做光学切片行组织学 测量RNFL厚度，将另外8只大鼠右眼做全视网膜铺片甲苯胺蓝染色，记数视网膜神经元细胞 密度，将结果进行比较分析。 结果:激光光凝后大鼠眼压缓慢、中等程 度升高，在第3、6、9 周时光凝眼眼压分别比对照眼眼压为显著升高，差异有统计学意义(P＜0.001)。 OCT检查结果显示在3、6、9周时大鼠光凝眼视盘RNFL厚度分别小于对照眼，差 异有统计学意义（P＜0.05）。处死大鼠后组织学测量RNFL厚度，在3、6、9周时，光 凝眼为（64.38±6.54）、（51.47±6.4）、（42.10±6.10）μm，对照眼厚度为（76.23±6.78）、（78.64±6.15）、（77.64±6.63）μm。将两种方法测 得RNF L厚度值进行回归分析，两者变化趋势一致，相关系数(R=0.932，P＜0.001)。全视网 膜铺片甲胺蓝染色结果显示两组视网膜神经元细胞（RGC）密度值差异有统计学意义（P＜0.0 5）。 结论:激光光凝大鼠小梁可以成功建立大鼠慢性高眼压模型；OCT对大鼠慢性高眼压模型视盘RNFL厚度的测量与 在光学显微镜下的测量值变化趋势一致，相关性好；OCT可以连续活体监测大鼠慢性高眼压 模型视盘神经纤维厚度变化，从而了解大鼠青光眼视神经病变的进展。     

近视眼屈光度与眼压视盘参数的关系

目的探讨近视眼的屈光度与眼压、视盘参数之间的关系。方法通过海德堡视网膜断层扫描仪II型(HRT-II)获得65例患者96眼的视盘地形图测量,将96眼根据屈光度分为3组,每组32眼,低度近视≤-3.00D;中度近视-3.00~-6.00D;高度近视≥-6.00D,分析每组屈光度与眼压、视盘参数之间的关系。结果高度近视组的视网膜平均神经纤维层厚度较其他组明显变薄,在统计学上有显著性差异(其中高、中度近视组间P=0.01,高、低度近视组间P=0.00);眼压较其他组高,具有统计学意义(其中高、中度近视组间P=0.04,高、低度近视组间P=0.03;中、低度近视组间无明显差异);高度近视组中随着屈光度的增加视网膜平均神经纤维层厚度有明显变薄趋势(r=-0.504,P<0·001),眼压有轻度上升的趋势(r=0.377,P=0.005),此种趋势在其他组中未见到。结论对于高度近视眼视网膜神经纤维层厚度的长期随访有助于早期青光眼的发现。     

应用3D-OCT对不同角膜厚度的高眼压症患眼CP-RNFL和视盘及黄斑区参数的研究

目的:观察不同中央角膜厚度(CCT)的高眼压症(OHT)患者环视盘神经纤维层厚度(CP-RNFL)、视盘及黄斑区参数的差异,并与正常人群对比,探讨CCT与各参数的关系。方法:前瞻性临床病例对照分析。纳入2016-01/2019-01在广东医科大学附属医院眼科确诊的OHT患者77例124眼进行研究。所有患者均未曾用药治疗。依据CCT的厚度分为3组:组1(CCT<555μm)25例38眼,组2(CCT 555~590μm)26例44眼,组3(CCT>590μm)26例42眼,选取同期年龄、性别、眼别均与高眼压组相匹配的健康体检者77例124眼为正常对照组。所有受检者均行视盘及黄斑三维光相干断层扫描(OCT)检查。运用系统自带软件计算平均CP-RNFL及各象限CP-RNFL的厚度及视盘、黄斑区各参数。结果:组1的OHT患者比正常对照组盘沿面积变小;相比组2,组3的患者,其下方CP-RNFL厚度变薄,盘沿的面积变小;相比组3的患者,其黄斑区内环颞侧视网膜厚度变薄。三组高眼压组患者的黄斑中心凹、中心1mm、内环颞侧视网膜厚度较正常对照组变薄;CCT与盘沿面积呈正相关(均P<0.05)。结论:尽管OHT患者的RNFL和视盘及黄斑区各参数在正常范围,但与正常人群对比还是有差异;CCT<555μm可能是OHT向开角型青光眼(POAG)转变的危险因素,临床上需要加强随诊及早期干预。     

慢性高眼压对兔眼视神经的影响

本实验对２２只（４４只眼）健康成年青紫蓝兔的视神经乳头，在持续不同时间的高眼压状态下，分别进行了光镜和电镜的观察。     

兔慢性长期性高眼压模型建立

目的 建立家兔长期稳定性慢性高眼压模型.方法 将14只兔随机分为A、B两组,每组7只兔(14只眼).A组把长3 mm、宽2 mm的一次性输液管片从角巩膜缘植入前房;B组向前房内注入玻璃酸钠0.2 ml,术后不同时段对两组高眼压模型进行观察.结果 A组兔眼眼压术后7 d开始升高,持续升高至实验结束(观察2个月),平均眼压(32±4.37)mm Hg,最高峰值(35±3.58)mm Hg,模型建立成功率92%;B组100%兔眼眼压升高,但只能持续1～2 d,出现周边角膜膨出、角膜变形等并发症;3 d时无1眼眼压升高.结论 兔角巩膜缘植入一次性输液管材料能建立慢性长期性高眼压模型.     

棕色挪威鼠慢性高眼压性青光眼模型

目的建立高渗盐水诱导的棕色挪威鼠慢性高眼压性青光眼模型.方法23只棕色挪威鼠23眼.使用玻璃微针头将50微升1.75M高渗盐水注入实验眼的巩膜表面静脉.动物在清醒状态下,定期测量眼压及角膜直径以及眼底视神经乳头情况,并将其分别与同期对侧对照眼比较.结束观察后,剜出鼠眼,行组织病理检查.结果高渗盐水注射后,17只鼠眼发生了明显的眼压升高.10眼发生了眼球扩大(角膜直径增大超过1mm),且出现了明显的杯凹(平均杯盘比值为0.83±0.12),角膜扩大与杯凹出现的时间基本相同.结论采用1.75M高渗盐水能成功诱导出鼠眼慢性眼压升高,并产生确定的类似人类青光眼的视神经乳头杯凹.     

Effect of ATP-sensitive Potassium Channel Openers on Intraocular Pressure in Ocular Hypertensive Animal Models

PurposeTo evaluate the effect of ATP-sensitive potassium channel openers cromakalim prodrug 1 (CKLP1) and diazoxide on IOP in three independent mouse models of ocular hypertension.MethodsBaseline IOP was measured in TGFβ2 overexpression, steroid-induced, and iris dispersion (DBA/2J) ocular hypertension mouse models, followed by once daily eyedrop administration with CKLP1 (5 mM) or diazoxide (5 mM). The IOP was measured in conscious animals with a handheld rebound tonometer. Aqueous humor dynamics were assessed by a constant perfusion method. Effect of treatment on ocular tissues was evaluated by transmission electron microscopy.ResultsCKLP1 decreased the IOP by 20% in TGFβ2 overexpressing mice (n = 6; P < 0.0001), 24% in steroid-induced ocular hypertensive mice (n = 8; P < 0.0001), and 43% in DBA/2J mice (n = 15; P < 0.0001). Diazoxide decreased the IOP by 32% in mice with steroid-induced ocular hypertension (n = 13; P < 0.0001) and by 41% in DBA/2J mice (n = 4; P = 0.005). An analysis of the aqueous humor dynamics revealed that CKLP1 decreased the episcleral venous pressure by 29% in TGFβ2 overexpressing mice (n = 13; P < 0.0001) and by 72% in DBA/2J mice (n = 4 control, 3 treated; P = 0.0002). Diazoxide lowered episcleral venous pressure by 35% in steroid-induced ocular hypertensive mice (n = 3; P = 0.03). Tissue histology and cell morphology appeared normal when compared with controls. Accumulation of extracellular matrix was reduced in CKLP1- and diazoxide-treated eyes in the steroid-induced ocular hypertension model.ConclusionsATP-sensitive potassium channel openers CKLP1 and diazoxide effectively decreased the IOP in ocular hypertensive animal models by decreasing the episcleral venous pressure, supporting a potential therapeutic application of these agents in ocular hypertension and glaucoma.     

The Circadian Variations in Systemic Blood Pressure, Ocular Perfusion Pressure, and Ocular Blood Flow: Risk Factors for Glaucoma?

Intraocular pressure, a major risk factor for glaucoma, is known to vary throughout the day, yet glaucoma continues to progress in some patients despite it being well controlled. It is important to understand how other glaucomatous risk factors are affected by circadian variations. The purpose of this review is to analyze the literature concerning circadian variations in systemic blood pressure, ocular perfusion pressure, and ocular blood flow and to identify consensus findings regarding their impact on glaucoma. This review suggests that nonphysiologic nocturnal blood pressure dipping and wider circadian fluctuations in ocular perfusion pressure are linked with the development and progression of glaucoma. No consensus concerning circadian variations in ocular blood flow exists in the current literature, and future investigations of nocturnal changes in blood flow and glaucoma progression are required.     

The influence of sex difference in measurements with the Langham Ocular Blood Flow System

PURPOSE: To assess sex difference and parameters possibly accounting for such a difference in healthy subjects evaluated by means of the Langham Ocular Blood Flow (OBF) System.Methods: Pulse amplitude of intraocular pressure (IOP) and pulsatile ocular blood flow (POBF) as measured with the Langham OBF System were assessed in 86 healthy men and 69 healthy women. RESULTS: Compared to men, women showed higher POBF (mean +/- SD: 722.6 +/- 152.8 versus 647.8 +/- 164.9 microL/min; P =.0056) and pulse amplitude (mean +/- SD: 2.3 +/- 0.7 versus 2.0 +/- 0.6 mm Hg; P =.0043) values. Sex difference was still significant after correcting for age, refraction, blood pressure, IOP, and pulse rate. Pulse amplitude correlated negatively with pulse rate, and POBF correlated negatively with IOP. Women had higher readings in pulse amplitude and POBF, even after correcting for age, refraction, IOP, blood pressure, and pulse rate. CONCLUSIONS: While using the Langham OBF System, one needs to be aware of sex difference that is independent of other hemodynamic parameters. How the observed difference in POBF is related to ocular blood flow, and how it might influence the preponderance of various ocular diseases in men or women remains to be clarified.