西藏高原地区LASIK治疗近视过矫的临床分析

目的:探讨西藏高原地区影响准分子激光原位角膜磨镶术(laser in situ keratomileusts,LASIK)治疗近视过矫的因素及解决办法。方法:对126例252眼近视患者中LASIK术后明显过矫的32例58眼术前、术后的相关资料进行分析。结果:术后2mo过矫者32例58眼(23.0%),裸眼视力0.5~0.8,过矫范围+1.50~+2.25DS,主观插片均≥1.0;术后6mo过矫者5例7眼(2.8%),裸眼视力0.8~1.0-2,过矫范围+0.75~+1.25DS,主观插片均≥1.0。其中过矫的患者术前角膜厚度500~563μm,术前屈光度数为-5.00~-7.50D,散光-1.50~-2.75DC,术前最佳矫正视力≥1.0。结论:我院LASIK手术治疗近视过矫患者较多,恢复时间较长,可能与当地海拔、温度、湿度、手术参数及患者的配合情况等因素有关。     

单眼行LASIK或LASEK术后疗效观察

目的:探讨单眼行准分子激光原位角膜磨镶术(laserin situkeratomileusis,LASIK)或准分子激光上皮下角膜磨镶术(laser epithelial keratomileusis,LASEK)治疗单眼近视所致屈光参差的效果。方法:采用对单眼等效球镜度>-2.50D的近视性屈光参差患者62例,进行单眼LASIK或LASEK手术。术眼及非术眼手术前后平均屈光度、屈光参差度数、最佳矫正视力和裸眼视力进行评价,术后随访6~24mo。结果:术眼术前平均等值球镜度数为-3.66(-2.50~-6.25)D,术后减少至-0.62(0.00~-1.00)D。LASIK或LASEK对平均等值球镜改变为-3.38(-2.50~-5.50)D。术前两眼平均屈光参差为-3.25(-2.50~-6.25)D,术后减少至-0.85(0.00~-1.75)D。术前术后最佳矫正视力(BCVA)范围均为0.6~1.0,平均最佳矫正视力从术前0.8提高到1.04;术后裸眼视力≥1.0者59眼,平均裸眼视力从术前的0.1提高至术后的1.0。非术眼术前平均等值球镜度数为-0.85(+0.25~-1.50)D,术后平均等值球镜度数为-1.85(-0.50~-3.50)D,平均裸眼视力从术前的0.5术后下降至0.1。结论:单眼LASIK或LASEK治疗近视性屈光参差虽然能提高患眼的最佳矫正视力和裸眼视力,解除单眼近视、散光所致的屈光参差对眼镜或角膜接触镜不能耐受的痛苦,而且对恢复双眼单视功能具有积极意义,但是同时我们也发现术后非术眼有近视加深的趋势,而且非术眼原近视度数越高近视加深越快越多。     

角膜塑形术矫治不同屈光度青少年近视的临床观察

目的：观察角膜塑形术（orthokeratology）在控制或减缓不同屈光度青少年近视发展作用方面的差异。方法：选用美国欧普康视角膜塑形镜（OK contact lens）,屈光度为-1.00～-5.00DS（等效球镜）、散光度≤-1.50DC的169例316眼青少年近视患者进行矫正后,依据屈光度平均分为4组,Ⅰ组-1.00～-2.00DS,Ⅱ组-2.25～-3.00DS,Ⅲ组-3.25～-4.00DS,Ⅳ组-4.25～-5.00DS,在6,12,24mo后,根据裸眼视力≥1.0和≥0.8的患者结果进行统计分析。结果：配戴角膜塑形镜6mo后：Ⅰ组和Ⅱ组的裸眼视力≥1.0分别为100%和96.2%,Ⅲ组≥1.0的93.6%,Ⅳ组≥1.0的88.6%。在配戴12mo后：Ⅰ组≥1.0的87.3%,≥0.8的12.7%;Ⅱ组≥1.0的84.8%,≥0.8的15.2%;Ⅲ组≥1.0的77.2%,≥0.8的22.8%;Ⅳ组≥1.0的70.9%,≥0.8的29.1%。在24mo后：I组≥1.0的59.5%,≥0.8的15.2;Ⅱ组≥1.0的54.4%,≥0.8的19.0%;Ⅲ组≥1.0的53.2%,≥0.8的13.9%;Ⅳ组≥1.0的45.6%,≥0.8的10.1%。结论：角膜塑形术在控制或减缓青少年近视发展的效果与配戴患者的屈光度增加成负相关,在中低度组配戴患者中,控制或减缓近视发展的效果优于高度组,因此对于早期中低度近视的青少年可以选择角膜塑形术,角膜塑形术在控制或减缓青少年近视方面具有起效快、无创性及塑形可逆的优点,在控制或减缓青少年近视发展方面是一种可以选择的方法。     

SBK治疗近视临床观察

目的:探讨准分子激光前弹力层下角膜磨镶术(subBowman’s keratomileusis,SBK)治疗近视的临床疗效。方法:回顾2009-12/2010-06间采用SBK治疗近视患者71例142眼的术前及术后6mo的视力、屈光度和角膜前后表面高度的变化。结果:术后6mo患者裸眼视力0.8~1.5,平均1.14±0.17,所有患者UCVA均≥0.8,UCVA≥1.0者136眼(95.8%),UCVA≥1.2者64眼(45.1%);术后6mo最佳矫正视力(BCVA)除2例3眼较前下降1行外,其余与术前相同或提高,BCVA均≥0.8,BCVA均≥1.0者136眼(95.8%),BCVA≥1.2者70眼(49.3%),术后6mo64眼(45.1%)UCVA≥术前BCVA。屈光度:术后6mo等效球镜(SE)为-0.65~+0.97(平均0.15±0.41)D。SE均≤±1.00D,92.8%≤±0.5D。术后6mo观察角膜前后表面高度变化大致相同。结论:SBK治疗近视有良好的预测性、准确性及安全性。     

角膜塑形矫治不同年龄段青少年近视的临床观察

目的:观察角膜塑形术(orthokeratology)在控制或减缓不同年龄段青少年近视发展的差异。方法:选用美国欧普康视角膜塑形镜(OK contactlens),对于年龄在7～18岁、屈光度为(等效球镜)-1.00～-5.00DS、散光度≤-1.50DC的212例315眼青少年近视患者进行矫正后,依据年龄平均分为4组,在6,12,24mo后,根据裸眼视力≥1.0和≥0.8的患者结果进行统计分析。结果:配戴角膜塑形镜6mo后,四组患者的裸眼视力均≥1.0,患者在配戴12mo后,I组≥1.0的38.2%,≥0.8的61.8%;Ⅱ组≥1.0的54.0%,≥0.8的46.0%;Ⅲ组≥1.0的62.2%,≥0.8的37.8%;Ⅳ组≥1.0的100%。在24mo后,I组≥1.0的7.3%,≥0.8的8.9%;II组≥1.0的21.6%,≥0.8的15.8%;III组≥1.0的37.8%,≥0.8的16.2%;Ⅳ组≥1.0的62.5%,≥0.8的37.5%。结论:角膜塑形术在控制或减缓青少年近视发展的效果与配戴患者的年龄增加成正比,配戴患者年龄越大,控制或减缓近视的效果越明显,角膜塑形术在控制或减缓青少年近视方面具有起效快,无创性及塑形可逆的优点,是青少年近视的一种可供选择的方法。     

LASIK矫正体表瘢痕疙瘩者近视的临床研究

目的：研究和观察准分子激光原位角膜磨镶术（LASIK）治疗体表伴瘢痕疙瘩近视患者的安全性、有效性和预测性。方法：前瞻性连续研究,在伦理委员会同意下,对16例32眼体表有瘢痕疙瘩的近视患者行LASIK矫正,年龄19～29（平均23.6）岁,裸眼远视力0.05～0.2,最佳矫正视力0.8～1.2,常规行裂隙灯显微镜,OrbscanⅡ眼前节分析系统、眼压、角膜厚度、电脑验光、散瞳检影、主观验光、对比敏感度和眩光等检查。患者均先行1眼手术,术后3mo无异常反应者再行对侧眼,术后随访2～6a,平均58.20±4.6mo。结果：术后2～6a,裸眼视力≥1.0者30眼（94%）,0.8者2眼（6%）。术后最佳矫正视力高于或等于术前者31眼（97%）,1眼有-0.75D屈光回退,术后屈光度与目标屈光度的差值平均为-0.25±0.35（-0.75～＋0.75）DS。角膜透明,层间无haze形成及瘢痕愈合,无角膜扩张及角膜明显增厚。结论：LASIK治疗瘢痕疙瘩近视患者安全、有效;同时也说明,角膜瓣与基质层间愈合非瘢痕性愈合,但需大样本长期随访进一步证明。     

LASIK治疗近视合并中高度散光临床观察

目的:探讨准分子激光原位角膜磨镶术(LASIK)治疗近视合并中高度散光的安全性和有效性。方法:应用德国Wavelight公司的鹰视准分子激光治疗系统对62例83眼近视合并中高度散光(≥-2.00D)患者进行LASIK治疗。随访6mo,比较手术前后的视力、屈光度、散光及其散光轴位的变化。结果:术后6mo,视力在0.8以上(≥0.8)和1.0以上(≥1.0)者分别为78%和47%,裸眼视力≥术前最佳矫正视力(BCVA)57眼(69%),散光度数在±1.00以内64眼(77%),残留散光平均为-0.80D,散光矫正(±0.50以内)37眼(45%)。结论:LASIK治疗近视合并中高度散光效果明显,患者术后满意度高。     

飞秒激光联合LASIK术后明暗环境下对比敏感度的变化

目的：：对比飞秒激光联合准分子激光角膜原位磨镶术( femtosecond-Laser in situ keratomileusis, femto-LASIK)与准分子激光原位角膜磨镶术( Laser in situ keratomileusis, LASIK)治疗近视和近视散光手术后术眼在明、暗环境下对比敏感度( contrast sensitivity,CS)的变化。方法：选择2010-01/2012-02于沈阳市第四医院眼科接受femto-LASIK术( A组)或LASIK术( B组)的近视及近视散光患者各80例80眼,近视度数在-1.50~-10.00D,散光度≤-6.0D,矫正视力≧1.0的患者,跟踪随访6mo,常规记录裸眼视力、最佳矫正视力、客观验光值、裂隙灯检查、术后有无并发症、眼压、角膜地形图等,术前术后行明环境下和暗环境下CS检查,比较两组明暗环境下CS的变化。结果：研究对象160例中,所有患者手术均成功, femto-LASIK术组( A组)术后明暗环境下各空间频率的CS均高于标准LASIK术组( B组)。其中A组术后1 mo明视CS、术后3 mo暗视CS均恢复至术前水平,术后6 mo时均较术前提高;B组术后3 mo明视CS达术前水平,暗视CS术后6 mo时仍没恢复至术前水平。结论：femto-LASIK术矫正近视和近视散光,在提高术后明暗环境下CS比标准LASIK术更有优势。     

大龄近视患者准分子激光原位角膜磨镶术分析

目的　探讨大龄近视患者LASIK疗效、特点及需要加以关注的问题。方法　对 88例(16 4眼 )大龄 (年龄≥ 4 0岁 )近视患者进行LASIK治疗 ,并对术前屈光度、预矫屈光度、手术疗效等进行统计分析。结果　行LASIK治疗的大龄近视患者术前屈光度 (球镜等量 ) :轻度近视 (≤ -3D) 5眼 ,占 3% ,中度近视 (>- 3D ,≤ - 6D) 2 8眼 ,占 17% ,高度近视 (>- 6D ,≤ - 10D) 4 2眼 ,占 2 6 % ,超高度近视 (>- 10D) 89眼 ,占 5 4 %。为保证角膜的安全性 ,2 0例 (2 2 73% ) 39眼(2 3 78% )术前设计的预矫屈光度需低于术前屈光度。术后裸眼视力 0 0 6～ 1 5 ,平均 0 78± 0 39,其中裸眼视力≥ 0 5者为 6 1眼 ,占 78 2 1% ,裸眼视力≥ 1 0者 2 5眼 ,占 32 0 5 %。结论　大龄近视患者行LASIK治疗以高度、超高度近视患者为主 ,术前角膜厚度的仔细测量、预矫屈光度数的确定、激光切削直径的选择对减少眩光以及术后屈光度数回退 ,提高术后视力、改善视觉质量至关重要。     

FEMTO LDV飞秒激光制瓣LASIK术治疗近视疗效观察

目的：评价FEMTO LDV飞秒激光制瓣准分子激光原位角膜磨镶术(laser in situ keratomileusis,LASIK)治疗近视的临床效果。

方法：应用FEMTO LDV飞秒激光制瓣,设定角膜瓣厚度110μm。EC5000-CXIII准分子激光仪行LASIK手术治疗近视患者143例283眼。术前检查包括验光、最佳矫正视力(best corrected visual acuity,BCVA)、角膜厚度、ObscanⅡ等。术中测量其中35眼的角膜床厚度,推算其角膜瓣的厚度。观察术中及术后角膜瓣情况,手术并发症,术后裸眼视力(uncorrected visual acuity,UCVA),屈光度,角膜地形图,平均随访3mo。

结果：术中出现过小瓣(直径<5mm)3眼,角膜边缘切开不完全5眼,切口出血8眼,术后球结膜下出血6眼。35眼角膜瓣厚度108.75±8.52(98～117)μm,误差(实测值与预设值之差)6.49±8.62(3～12)μm,实际角膜瓣厚度与术前预先设计的角膜瓣厚度差异无统计学意义(P>0.05)。术后3mo平均等效球镜-0.29±0.47(-1.50～+1.00)DS,251眼(88.7%)裸眼视力达到或超过术前最佳矫正视力。

结论：FEMTO LDV飞秒激光制瓣LASIK术治疗近视并发症少、疗效确切、安全。     

Follow-up studies in pattern VECP in demyelinating diseases in children

Spectral sensitivity functions and the transient decrease of sensitivity to short wavelengths after the offset of yellow light (transient tritanopia) were measured by increment threshold techniques in patients suffering from hereditary macular degenerations. Color vision defects were determined by arrangement tests and the anomaloscope. Central areolar choroidal dystrophy was found to produce a mild protan defect and to reduce foveal spectral sensitivity throughout the visible spectrum by a factor of 100; it also abolishes transient tritanopia. Electroretinogram (ERG) was normal, electrooculogram (EOG) subnormal. Stargardt's disease, despite numerous fluorescent macular spots, does not abolish transient tritanopia nor does it reduce spectral sensitivity, although scotopic matches were performed on the Nagel anomaloscope. Only in severe, advanced cases was transient tritanopia reduced and spectral sensitivity found to follow the absorption spectrum of rods. Routine ERGs and EOGs were normal. Vitelliform macular degeneration, despite the ophthalmoscopically pronounced dystrophic macula, produced only very small changes in spectral sensitivity and transient tritanopia, although a widened matching range on the Nagel anomaloscope and electrophysiological abnormalities were found. Apparently damage of the retinal circuit which connects long and short wavelength-sensitive cones, caused by hereditary conditions, is different from that caused by retinotoxic drugs.     

p53 expression in pterygium in two climatic regions in Turkey

Purpose:

To assess accumulation of p53 protein in samples of primary pterygium from people living in two different climatic regions in Turkey.

Materials and Methods:

Group 1 included 101 pterygium specimens from people in Adana located in southern Turkey. Group 2 included 39 pterygium specimens from people in Ankara, located in the middle of Turkey. Climatic conditions throughout the year are sunnier and warmer in Adana than they are in Ankara. The control group (Group 3) included 30 specimens of conjunctiva that had been excised during cataract surgery from 30 patients without pterygium. The pterygial specimens and control conjunctiva were studied by immunohistochemistry using antibodies against p53 protein. Pearson''s chi-square test was used to compare the p53 immunoreactivity.

Results:

The p53 immunoreactivity in Groups 1 and 2 was greater than it was in the control group (P<0.001). There were no differences in p53 immunoreactivity between Groups 1 and 2 (P= 0.060).

Conclusion:

The p53 immunoreactivity was not correlated with ultraviolet irradiation exposure. The p53 immunoreactivity in our pterygium specimens suggests that pterygium could be a result of uncontrolled cell proliferation.     

Changes in Bruch's membrane in experimental hypercholesteremia in rats

PURPOSE: We investigated the effect of high cholesterol diet for the aging changes in Bruch's membrane of rats. METHODS: After feeding a 4% cholesterol diet for 15 weeks to three young rats 3 months old and four aged rats 23 months old, we observed the morphological changes of Bruch's membrane by electron microscopy, and made a comparison with rats fed an ordinary diet. RESULTS: In one young rat fed a high-cholesterol diet, the endothelial basement membrane of the choriocapillaris formed multiple folds separated from the plasma membrane of the endothelium and showed lamellar thickening and crack in some areas. The elastic fiber layer in Bruch's membrane disappeared partly and some new microfibrils appeared. In one aged rat fed a high-cholesterol diet, the endothelial basement membrane of the choriocapillaris showed more lamellar thickening with lumps in some parts. Compared with rats fed an ordinary diet, rats fed a high-cholesterol diet showed thickening of the basement membrane and the changes were more severe. CONCLUSIONS: Our data indicated that high-cholesterol diet might promote age-related changes of Bruch's membrane.     

Trends in Patterns of Anterior Uveitis in a Tertiary Institution in Singapore

Purpose: To report the trends in etiology of patients with anterior uveitis (AU) in Singapore over 6 years.

Methods: A retrospective review of the clinical records of all new patients who presented with anterior uveitis to the uveitis subspecialty clinic from 2005 to 2010 at Tan Tock Seng Hospital, Singapore.

Results: There were 552 new cases of AU. This comprised 59.5% of a total of 928 new patients diagnosed with uveitis from 2005 to 2010. The mean age was 48.0?±?17.2 years. There was a male predominance (62.5%), with a male:female ratio of 1.7:1. The majority were of Chinese ethnicity (69%), followed by Malays (13.2%). Most cases were unilateral (79.5%) and idiopathic (50.4%). Common etiological causes included Fuchs heterochromic iridocyclitis (FHI) (5.6%), ankylosing spondylitis (AS)-related AU (5.1%), herpes simplex virus (HSV) (4.7%), and herpes zoster virus (HZV) (4.5%). There were increasing trends in AS-related AU from 3.2% in 2008 to 6.5% in 2010, and psoriasis-associated AU from 1.7% in 2005 to 4.0% in 2008. There were decreasing trends in the incidence of FHI from 10.6% in 2006 to 4.7% in 2009. No change in incidence of viral etiologies was noted, but cytomegalovirus-related immune-recovery uveitis (IRU) comprised 7.4%. IRU showed an increasing trend from 1.7% in 2005 to 11.9% in 2007, then decreased to 3.3% in 2010. Using the Pearson chi-square test, there was no statistically significant association between ethnicities (Chinese, Malay, Indian) comparing infectious and noninfectious cases (p?=?0.788), idiopathic and nonidiopathic cases (p?=?0.170), or between the various etiologies of uveitis (p?=?0.168).

Conclusions: AU was the predominant form of uveitis seen at our centers. Infectious etiologies (18.5%) are the most common among nonidiopathic cases, with herpes viruses (9.2%) being most prevalent. Despite increased use of polymerase chain reaction (PCR) in the detection of microbial and viral DNA, there was no overall increase in detection of infectious causes for uveitis. The changes in CMV-related immune recovery uveitis from 2005 to 2010 could reflect a change in HIV management in Singapore.     

实验性糖尿病视网膜微血管病变的病理研究

目的：观察糖尿病视网膜病变（diabetic retinopathy,DR）的组织学改变。方法：应用光镜、免疫组织化学、电镜及组织化学电镜等技术,研究在不同时间点Spregue-Dawley(SD)大鼠视网膜毛细血管基底膜中的Ⅳ型胶原蛋白及层黏蛋白和视网膜毛细胞血管基底膜的厚度,以及其负电荷位点数目的变化。结果：随着糖尿病病程的发展,视网膜毛细血管基底膜下不断增厚伴有Ⅳ型胶原蛋白及层黏蛋白的增加,同时负电荷位点数目减少。结论：视网膜毛细血管基底膜增厚,Ⅳ型胶原蛋白及层黏蛋白的增加,负电荷位点数目减少可能是导致DR渗出性病变的病理基础。     

Orthokeratology practice in children in a university clinic in Hong Kong*

Purposes: The aim of this study was to analyse clinical data of children undergoing orthokeratology (ortho‐k) and to investigate patients’/parents’ perspective on ortho‐k via telephone interviews. Methods: Clinical records of children undergoing ortho‐k from a university optometry clinic were reviewed and the effects of ortho‐k on refraction, vision and cornea were investigated. A telephone interview was conducted to solicit patients’/parents’ perspective of the treatment. Results: One hundred and eight files were reviewed. Median age of the children was nine years (range six to 15); mean (±SD) pre‐treatment refractive sphere was ‐3.56 ± 1.49 D and the median refractive cylinder was ‐0.50 D (range zero to ‐4.25 D). Significant refractive spherical reduction (58 per cent), improvement in unaided vision and corneal topographical changes were noted after only one night of wear. No significant change in astigmatism was found. Corneal staining was the most commonly observed complication with ortho‐k and more than 80 per cent of patients were advised to apply ocular lubricants to loosen the lens before lens removal. Ortho‐k was mainly undertaken for myopic control and about 90 per cent of the respondents reported good/very good unaided vision after ortho‐k and ranked the treatment as satisfactory or very good. Lens binding and ocular discharge were the most frequently reported problems during the treatment. Conclusion: Under close monitoring, overnight ortho‐k is effective and safe for reducing low to moderate myopia and the treatment is well accepted by the children.     

内毒素诱导的大鼠葡萄膜炎的巨噬细胞中Toll样受体4的表达

目的 探讨在内毒素诱导的Wistar大鼠葡萄膜炎中Toll样受体4(TLR4)阳性细胞与虹膜组织中巨噬细胞的动态变化和分布.方法 实验研究.Wistar大鼠50只,用随机数字法随机分为5组,每组10只,分别为正常对照(0 h)组、6 h组、12 h组、24 h组及48 h组.除0 h组外其余各组均足垫部注射霍乱弧菌内毒素200μg,注射后于裂隙灯显微镜下观察双眼前节炎症反应变化.按实验分组于0、6、12、24、48 h处死大鼠.取虹膜一睫状体及脉络膜组织.通过葡萄膜铺片免疫组织化学方法检测TLR4和巨噬细胞的标记CD163的表达.人工计数虹膜中TLR4~+与CD163~+的细胞并计算细胞密度,计算圆形和多形性的CD163~+细胞占所有CD163~+细胞的百分比.进一步采用免疫荧光双标记检测TLR4和CD163共表达的情况.通过单因素方差分析分别对大鼠虹膜内阳性细胞密度以及圆形、多形性CD163~+细胞的百分比进行统计学检验.结果 正常大鼠虹膜睫状体组织不表达TLR4.6 h组有2只大鼠虹膜内可见少量TLR4~+细胞,12～48 h组所有大鼠虹膜内TLR4~+细胞明显增多(F=167.2,P＜0.001),虹膜内TLR4~+细胞密度分别为(506.1±39.5)个/mm~2(12 h组)、(492.3±54.5)个/mm~2(24 h组)及(663.8±150.2)个/mm~2 (48 h组).在注射LPS后12～48 h期间TLR4~+细胞形态无明显变化.0～48 h组大鼠虹膜内均有CD163~+细胞,0 h组圆形和多形性CD163~+细胞百分比为13%,12～48 h组其百分比约为80%,且圆形细胞主要位于虹膜基质层.免疫荧光双标记可见TLR4和CD163的共表达,TLR4位于细胞膜,CD163位于细胞质.5组大鼠脉络膜内均未见TLR4表达.结论 内毒素诱导的大鼠葡萄膜炎中虹膜内TLR4表达增高,部分虹膜固有巨噬细胞表达TLR4.TLR4可能在葡萄膜炎的发生发展中起一定作用.     

Ischemia Induces Significant Changes in Purine Nucleoside Concentration in the Retina-Choroid in Rats

Adenosine, produced from the decomposition of adenosine triphosphate, is believed to provide protective effects during ischemia. On the other hand, adenosine metabolites may serve as precursors for oxygen free radical formation. The time course of formation of adenosine and its purine metabolites was studied during retinal ischemia in rats. Concentrations of adenosine and its purine nucleoside metabolites inosine, hypoxanthine, and xanthine in the retina-choroid of ketamine/xylazine-anesthetized rats were measured during retinal ischemia using high performance liquid chromatography. Quantitative measurements were made possible in the small tissue mass through the use of internal standards. Ischemia was induced by ligation of the central retinal artery. In each rat, one eye was ischemic while the other served as a non-ischemic control. Eyes were frozen in situ at 1, 5, 10, 20, 30, 60, and 120 min of ischemia. The retina-choroid was then removed from the frozen eyes and analysed. Significant increases in the concentrations of adenosine, inosine, and hypoxanthine in ischemic compared to control retina-choroid were detectable within 1 to 5 min of the onset of ischemia, and within 10 min for xanthine. Increase in adenosine concentration in ischemic relative to control retina-choroid plateaued at 30 min of ischemia, while inosine and hypoxanthine concentrations increased continuously. The increase in xanthine concentration was exponential throughout the measurement period. This study documented the time-related changes in purine nucleoside concentration during ischemia. Prolonged ischemia results in ongoing production of xanthine, which by serving as a precursor for oxygen free radical formation, could be a pathogenic factor in prolonged retinal ischemia.