匹罗卡品对兔眼葡萄膜巩膜途径作用的形态学研究

目的：从形态学方面探讨匹罗卡品对兔眼葡萄膜巩膜途径的作用。方法：通过前房内注入微量示踪剂异硫氰酸荧光素牛血清白蛋白（Fluorescein isothiiocyanate-bovine serum albumin,FITC-BSA),匹罗卡品点眼后2,4,6,8,10和12h各处死家兔2只,摘除眼球作冰冻切片,于荧光显微镜下观察并确定睫状体、脉张膜上腔、前、后巩膜和脉络膜的荧光强度等级,并于光镜下观察其组织结构改变。结果：匹罗卡品点眼后眼压下降,点眼后睫状体、脉络膜上腔和前巩膜荧光强度均显著减弱,后巩膜、脉络膜无明显变化。光镜观察见睫状肌细胞间隙缩小。结论：匹罗卡品通过收缩睫状肌而减少房水从葡萄膜巩膜途径排出。     

盐酸哌唑嗪点眼房水葡萄膜巩膜途径的形态观察

目的观察兔眼房水葡萄膜巩膜途径的形态，探讨选择性α１受体阻断剂盐酸哌唑嗪（ｐｒａｚｏｓｉｎ，ＰＺ）点眼对该途径的形态学影响。方法前房注入微量示踪剂异硫氰酸荧光素牛血清白蛋白（ｆｌｕｏｒｅｓｃｅｉｎｉｓｏｔｈｉｏｃｙａｎａｔｅ－ｂｏｖｉｎｅｓｅｒｕｍａｌｂｕｍｉｎ，ＦＩＴＣ－ＢＳＡ）于ＰＺ点眼后２，４，６，８，１０，１２ｈ各处死家兔２只，摘除双侧眼球作冰冻切片，荧光显微镜下观察并确定睫状体、脉络膜上腔、前后巩膜和脉络膜的荧光强度等级。光镜下观察其组织结构变化。结果ＰＺ点眼后眼压出现有统计学意义的下降。ＰＺ点眼后葡萄膜巩膜途径各部位的荧光强度均比对照组显著增强，光镜观察仅见ＰＺ组睫状肌细胞间隙扩大。结论ＰＺ点眼可使眼压下降，点眼后促进房水从葡萄膜巩膜途径排出，房水由睫状肌细胞间隙到脉络膜上腔后，主要经前巩膜排出，后巩膜及脉络膜排出较少。     

国产与进口盐酸哌唑嗪对家兔眼压及房水葡萄膜巩膜途径影响的比较

目的　通过兔眼局部分别滴用国产和进口选择性α1受体阻断剂盐酸哌唑嗪( prazosin ,PZ) ,比较其对眼压以及房水葡萄膜巩膜途径形态的影响 ,评估国产PZ的可用性及有效性。方法　正常家兔随机分为 1g·L-1国产PZ组、1g·L-1进口PZ组及生理盐水对照组 ,各组均单侧滴眼 ,观测处理眼及对侧眼在不同时间点眼压的变化。前房注入微量示踪剂异硫氰酸荧光素牛血清白蛋白 (fluoresceinisothiocyanate bovineserumalbumin ,FITC BSA)于PZ滴眼后 2、4、6、8、10h各处死家兔 2只 ,摘除双侧眼球作冰冻切片 ,荧光显微镜下观察并确定睫状体、脉络膜上腔、前后巩膜和脉络膜的荧光强度等级。光镜下观察其组织结构变化。结果　国产PZ及进口PZ与对照组相比 ,均可显著降低双眼眼压 ;国产PZ滴眼后处理眼眼压最大下降幅度为 9.36mmHg( 1kPa =7.5mmHg) ,对侧眼为5 .73mmHg ;进口PZ滴眼后处理眼眼压最大下降幅度为 8.92mmHg ,对侧眼为6 .92mmHg。 2组间相比 ,尽管各时间点降眼压幅度不同 ,但降眼压效果无显著性差异。PZ滴眼后葡萄膜巩膜途径各部位的荧光强度均比对照组显著增强 ,光镜观察发现睫状肌细胞间隙扩大。结论　国产PZ滴眼后通过促进房水从葡萄膜巩膜途径排出可使眼压下降 ,与进口PZ房水排出途径基本一致。国产PZ可以替代     

非穿透性小梁切除术房水葡萄膜巩膜途径的实验研究

目的　探讨非穿透性小梁切除术 (nonpenetratingtrabecularsurgeryNPTS)房水葡萄膜巩膜引流途径的形态学情况 ,进一步阐明其降压机制。方法　 2 0只兔 4 0眼随机分为实验组 (NPTS) ,对照组 (小梁切除 +虹膜根切术 )和正常组 ,术后 1周于正常组前房内注入微量示踪剂异硫氰酸荧光素牛血清白蛋白 (fluoresceinisothiocyanate bovineserumalbumin ,FITC BSA) ,于 2、4、6、8、10h各处死家兔 4只 ,摘除双侧眼球作冰冻切片 ,荧光显微镜下观察并确定睫状体、房水池、脉络膜上腔、前、后巩膜和脉络膜的荧光强度等级。结果　实验组和对照组术前眼压相似 (实验组 2 .19kPa± 0 .37kPa ,对照组 2 .0 0kPa± 0 .34kPa ;P >0 .0 5 ) ,术后 1周时眼压差别没有统计学意义 (实验组 1.5 1kPa± 0 .35kPa ,对照组 1.4 4kPa± 0 .31kPa;P >0 .0 5 )。实验组术后葡萄膜巩膜途径各部位的荧光强度均比正常组和对照组增强 ,而正常组亦强于对照组。结论　NPTS具有和小梁切除术相似的降压效果 ,房水由房水池和 (或 )睫状体间隙到脉络膜上腔后 ,主要经前巩膜排出 ,后巩膜及脉络膜排出较少 ,是其降压的主要机制之一。     

眼调节对葡萄膜巩膜房水外流途径影响的形态学观察

目的　通过形态学观察探讨眼调节对葡萄膜巩膜房水外流途径的影响。方法　14只健康日本大耳白兔,10只（20眼）用于荧光显微镜观察,4只（8眼）用于光镜观察,按用药方法不同各分为调节状态组和非调节状态组。所有白兔双眼分别采用5 g·L^-1硝酸毛果芸香碱滴眼液和10 g·L^-1盐酸环喷托酯滴眼液模拟眼调节态和非调节态,测量滴眼前及末次滴眼后30 min的眼压,于滴眼后30 min将5 μL异硫氰酸荧光素标记牛血清白蛋白（FITC-BSA）注入前房,于前房注射后0.5 h、1.5 h、2.5 h、3.5 h、4.5 h各处死2只白兔,摘取双眼作冰冻切片,于荧光显微镜下观察调节态和非调节态葡萄膜巩膜途径的房水荧光强度及其分布形态;于滴眼后30 min处死4只白兔,摘取双眼通过HE染色和抗平滑肌抗体染色在普通光镜下观察兔眼睫状肌形态、肌间隙。结果　调节状态组基线眼压（19.13±1.75）mmHg（1 kPa=7.5 mmHg),毛果芸香碱模拟眼调节后眼压下降,滴眼后眼压为（16.56±1.67）mmHg,差异有统计学意义（t=9.37,P=0.00)。调节状态组睫状体、脉络膜上腔和前巩膜荧光强度较非调节状态组均显著减弱（均为P<0.05）,而两组间后巩膜、脉络膜差异均无统计学意义（均为P＞0.05）。光镜观察见非调节状态组放射肌区域有明显肌间隙,而在调节状态组未发现此间隙。结论　眼调节可通过收缩睫状肌从而减少房水从葡萄膜巩膜房水外流道排出。     

非穿透性小梁手术对葡萄膜巩膜房水流出量的影响

目的探讨非穿透性小梁手术（nonpenetrating trabecular surgery，NPTS）对葡萄膜巩膜房水流出量的影响，从房水动力学的角度揭示NPTS降眼压的机制。方法用示踪剂异硫氰酸荧光素牛血清白蛋白（fluoresceinisothiocyanate—bovine serum albumin：FITC—BSA）于术后7d分别对手术后的兔眼模型组和正常兔眼组进行前房持续灌注30min，灌注毕处死家兔，摘除双侧眼球，并将组织分离为前巩膜、后巩膜、前葡萄膜、后葡萄膜、视网膜和残余液体等6种组织。测定每种组织的荧光强度，计算葡萄膜巩膜流出量（uveoscleral outflow，Fu）。结果实验组葡萄膜巩膜流出量明显高于正常组，两组前房水再现量均以前葡萄膜、前巩膜和残余液体为多，实验组术后葡萄膜巩膜通道各组织房水再现量与正常组相比差异有统计学意义（p〈0．001）。结论非穿透性小梁手术能增加葡萄膜巩膜途径房水流出量，房水主要由前巩膜排出。     

Lat-B对家兔房水葡萄膜巩膜引流通路的影响

目的:研究Lat-B对家兔眼内压、葡萄膜巩膜通路的影响。方法:兔眼局部应用Lat-B,BSS和DMSO,于用药前1h及用药后1,2,3,4,5,6,24h测量眼压后部分免疫荧光组通过前房内注入微量示踪剂异硫氰酸荧光素牛血清白蛋白(fluorescein isothiocyanate bovine serum albumin,FITC-BSA),于点眼后2,4,6,8,10h各处死家兔2只,摘除双侧眼球作冰冻切片,于荧光显微镜下观察并确定睫状体、脉络膜上腔、前、后巩膜和脉络膜的荧光强度等级。结果:Lat-B滴眼后处理眼眼压不同时间点与滴眼前比较眼压呈下降趋势,差异有显著性(P<0.05),1h即可引起眼压降低,24h仍有效,BSS组与DMSO组未引起眼压下降;葡萄膜巩膜途径通路3组之间在睫状体、脉络膜上腔、前、后巩膜和脉络膜的荧光强度,各部位均为Lat-B组最强,Lat-B与BSS组和DMSO组相比差异均有显著性(P<0.05),BSS组和DMSO组相比差异无显著性。结论:Lat-B能够有效降低眼压,1h即可起效,且24h仍有效。Lat-B可以增加葡萄膜巩膜途径通路的房水流出率,具有治疗青光眼的应用前景,尤其是正常眼压性青光眼、开角性青光眼。     

玻璃体切除联合不同睫状体复位术式的疗效观察

目的:观察玻璃体切除联合两种睫状体复位缝合手术方法治疗复杂性睫状体脱离的临床疗效.方法:回顾42例42眼经B超及超声生物显微镜(ultrasound biomicroscopy,UBM)检查存在睫状体脱离(离断口范围≥600),同时伴有晶状体、玻璃体、视网膜病变和眼外伤患者的临床资料.按照睫状体复位手术方式分为玻璃体切除联合睫状体巩膜间断缝合组20眼(A组)、玻璃体切除联合睫状体巩膜连续褥式缝合组22眼(B组).A组首先间断缝合巩膜睫状体,然后进行玻璃体切除术.B组首先进行晶状体玻璃体切除术,然后由巩膜表面进针进入玻璃体腔内连续褥式缝合睫状体组织.观察术后最佳矫正视力、术后眼压情况、睫状体复位情况及两组患者睫状体复位手术时间,并进行统计分析.结果:两组患者术后视力及眼压情况差异无统计学意义(P＞0.05),两组患者术后视力及眼压较术前差异有统计学意义(P＜0.05),两组患者睫状体复位成功率(A组90％,B组86.36％)差异无统计学意义(P＞0.05),两组患者睫状体复位手术时间差异有统计学意义(P＜0.05).结论:玻璃体切除联合两种术式复位缝合睫状体治疗复杂性睫状体脱离均安全有效,对于保留晶状体者适宜应用睫状体巩膜间断缝合方法,睫状体巩膜连续褥式缝合法适用于无晶状体眼、人工晶状体眼患者,对于广泛性睫状体脱离者更为简便.     

青光安颗粒剂对慢性高眼压兔眼眼内组织的保护作用

目的：探讨青光安颗粒剂对慢性高眼压兔眼眼内组织的保护作用。方法：采用光镜和电镜观察方法，通过与丹参组、模型组、正常对照组的比较，观察青光安颗粒剂对慢性高眼压兔眼角膜、巩膜静脉窦、虹膜睫状体、视网膜组织的影响。结果：模型组兔眼角膜、巩膜静脉窦有轻度异常改变，虹膜睫状体和视网膜组织病理改变明显；丹参组兔眼眼内各组织结构相对保存较好；而青光安颗粒剂组兔眼眼内各组织比丹参组保存得更好，其病理改变不明显。结论：青光安颗粒剂对慢性高眼压兔眼眼内组织结构具有保护作用     

实验性低眼压的药物治疗

利用下列方法:睫状体脉络膜膜脱离、视网膜脱离或睫状体剥离,使恒河猴产生实验性低眼压。于两天后,在最低眼压时,用电离子透入法将10%氯化乙酰甲胆硷沉积于角膜,每眼局部点用0.25%毒扁豆硷水杨酸盐眼膏。所有眼之眼压升至正常范围,则持续8～12小时。眼压的峰值,发生于用药后1～4小时。患有睫状体脉络膜脱离、视网膜脱离和睫状体剥离的眼,眼压分别较治疗前眼压值高7.2、6.8和11.3mmHg。在正常眼组里,这种药物联合法则引起眼压呈短暂的5.7mmHg降低。乙酰甲胆硷和毒扁豆硷升高眼压的机理,可能是由于刺激房水生成、减少葡萄膜巩膜流出或者两者兼而存在所引起。     

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.