内皮素-1在次声作用后大鼠视网膜损伤中的作用

目的 探讨内皮素—1在次声作用后大鼠视网膜损伤中的作用。方法 雄性SD大鼠25只，分为5组，每组5只，除未经次声作用的对照组外，余4组放入次声舱，经16Hz、130dB每日作用2h，分别于1、7、14和21d处死，采用硝酸镧灌注固定法制备电镜样品。取眼球做病理切片。用免疫组化检测不同时期内皮素的不同表达部位。结果 次声作用1d和对照组表现相似，内皮素—1在视网膜和脉络膜血管弱表达；7d主要表达在视网膜的外段，内段也有较弱的表达；而14d主要表达在内段，内核层和节细胞层阳性表达加强；21d视网膜各层表达均减弱。随着次声作用时间的延长，视网膜组织表现由外段向内段的损伤。电镜下，随次声暴露时间的延长，除7d外镧的渗入也逐渐加重，视网膜各层出现细胞水肿、细胞器肿胀、染色质浓缩边集、细胞变性坏死、细胞膜断裂和髓样等改变。结论 内皮素—1表达在视网膜损伤部位的早期，可能作为对损伤的一种修复反应。     

次声作用后大鼠视网膜电图改变的研究

目的探讨次声作用对大鼠视网膜电图(ERG)参数的影响。方法48只大鼠按暴露时间随机分为8组，每组6只，暴露于8Hz、130dR的次声压力舱中，每日2h。分为暴露1、4、7、11、14、18、21d组及正常对照组。暴露前后分别行视网膜电图(ERG)、振荡电位(OPs)检测。结果暴露组ERG各指标不同程度受损，振幅下降，并表现出由外至内的趋势。次声作用后1d，以a波振幅下降为主，在4d组和7d组，b波的下降幅度超过a波，随暴露时间进一步延长，∑OPs的振幅异常为主要变化。结论次声确可造成一定程度的视觉系统功能障碍，损害涉及多层次多部位，且有独特的发展规律。     

次声作用后大鼠视网膜组织中GFAP与VEGF的表达

目的：研究8Hz(110dB)次声作用对大鼠视网膜组织中GFAP和VEGF的蛋白表达变化情况。方法：把大鼠置于8Hz(110dB)的次声压力舱中，每天暴露2h,于0，1，7，14，21天后，以免疫组化法检测视网膜组织中的GFAP，VEGF的蛋白表达，结果：次声作用7天后大鼠视网膜组织中的GFAP和VEGF的表达显著增强（P＜0．05），14，21天后此2种蛋白的表达非常显著增强（P＜0．01），结论：8Hz(110dB)次声作用条件下可造成视网膜组织的一定影响，引起视网膜组织中胶质细胞，血管内皮细胞的增生，程度与作用时间呈正相关。     

次声作用对大鼠血视网膜屏障超微结构的损害

目的 观察次声作用对大鼠血视网膜屏障（blood-retinal barrier，BRB）超微结构和通透性的影响。 方法 20只大鼠按暴露时间随机分为5组，每组4只。暴露于16 Hz，130 dB的次声压力仓中，2 h/d，分别暴露0(对照组)、1、7、14、 21 d后摘除眼球，硝酸镧灌注固定法制备电镜样品,超薄切片,电镜观察。 结果 随次声暴露时间 的延长，BRB的损害加重，线粒体肿胀，内质网扩张，膜盘破坏，视网膜色素上皮(retinal pigment epithelium, RPE )细胞变形坏死，核膜扩张等都随暴露时间的延长而更加明显。镧在视网膜各层都有分布，随着暴露时间的延长，镧在各层的渗漏越来越多。 结论 次声可造成一定程度的 BRB通透性损害；随着 次声暴露时间的延长，损害更严重。 （中华眼底病杂志，2003，19：46-48）     

次声暴露对大鼠血视网膜屏障超微结构的损害

目的 观察次声暴露对大鼠血视网膜屏障超微结构和通透性的作用。方法 将15只Sprague-Dawley(SD）大鼠分为：实验组12只，给予8Hz,130dB基础噪音的次声暴露，2h/d，分别于暴露后1，7，14及21d，用20g/L戊巴比妥钠腹腔麻醉动物，10min后取其眼球，均以硝酸镧（La)作为示踪剂，采用镧苯滴注固定法制备电镜样品。对照组3只，亦置于次声舱中2h/d，但不接受次声暴露，结果 在次声作用下，暴露1d时La的渗漏无明显变化，7d时沉积在内节间，到达光感受器细胞核层，14d时在神经细胞间隙出现La颗粒，21d时到达神经及玻璃体，而形态学改变并不明显，主要是代谢方面的变化，如线粒体肿胀，内质网扩张，糖原颗粒的沉积，核周周隙增宽等。提示随时间的延长，血视网膜屏障的损害加重。结论 次声可影响一定程度的血视网膜屏障通透性，而致视觉功能损伤。     

糖尿病大鼠视网膜内皮素-1的表达

目的观察糖尿病大鼠视网膜内皮素-1(endothelin-1,ET-1)表达的影响。方法选取60只Wistar大鼠随机分为对照组和实验组。所有大鼠一次性腹腔注射0.1mol.L1链脲佐菌素诱发糖尿病模型。分别于成模后2周、4周、6周采用ADP酶视网膜铺片及免疫组织化学法分别观察视网膜血管的改变及检测视网膜ET-1的表达。结果与对照组相比,实验组大鼠6周时视网膜周边血管走形迂曲,神经节细胞排列紊乱,细胞数目减少,视网膜变薄。实验组大鼠视网膜ET-1表达随病程进展逐渐增强,4周、6周时平均积分光密度值分别为60.19±12.95、114.21±22.71,较同期对照组(15.35±8.38、15.22±4.71)增高,差异均有统计学意义(均为P<0.05)。结论随着糖尿病大鼠病程进展,视网膜ET-1表达逐渐增强。     

次声对大鼠视觉电生理和视网膜超微结构的影响

目的探讨8Hz(110dB)次声作用对大鼠视觉电生理功能及视网膜结构的影响.方法35只雄性成年大鼠随机分为7组,置于8Hz(110dB)的环境下,用视觉电生理(VEP、ERG、OPs)和形态学检查,检测视网膜的功能和结构.结果作用7天至21天后,见ERG的a波、b波的振幅下降,有显著差异(P＜0.05).光镜观察视网膜的组织形态学无明显变化.电镜观察首先出现视网膜外屏障、外颗粒层的损伤,随着作用时间的延长呈现内、外屏障及内、外颗粒层、神经节细胞层的损伤.结论8Hz(110dB)次声作用后,可造成大鼠视网膜结构和功能一定的影响,程度与作用次数呈直接相关.     

缬沙坦对糖尿病大鼠视网膜内皮素-1表达的影响

目的 观察缬沙坦对糖尿病大鼠视网膜内皮素-1(endothelin-1,ET-1)表达的影响.方法 选取90只Wistar大鼠随机平均分为对照组、高糖组和治疗组高糖组和治疗组大鼠一次性腹腔注射链脲佐菌素诱发糖尿病模型.成模后治疗组给缬沙坦按每天24 mg·kg-1灌胃,另外两组灌等体积蒸馏水.分别于干预后2周、4周、6周采用ADP酶视网膜铺片及免疫组织化学法观察视网膜血管的改变及检测视网膜ET-1的表达.结果 高糖组6周大鼠与对照组相比视网膜周边血管走形迂曲治疗组6周大鼠视网膜血管走形未见明显异常.治疗组大鼠视网膜ET-1表达在4周、6周时(平均积分光密度值分别为60.19±12.95、114.21±22.71)较同期对照组增高,但显著低于同期高糖组,差异具有统计学意义(P＜0.05).结论 缬沙坦能够降低糖尿病视网膜ET-1的表达,可能对糖尿病视网膜病变治疗起延缓作用.     

视网膜后膜的超微结构观察

在34例视网膜脱离伴增殖性玻璃体视网膜病变的慢性病例中，观察到12例视网膜后膜，占35.3%.其中对1例经玻璃体手术切除的标本进行了透射电镜检查。神经胶质细胞、视网膜色素上皮细胞及大量胶原纤维是后膜的主要细胞或间质成分。 （中华眼底病杂志，1994，10：165-166）     

糖尿病视网膜病变患者血浆内皮素-1的变化及意义

糖尿病视网膜病变患者血浆内皮素－１的变化及意义何剑峰鲍连云仇宜解为探讨糖尿病视网膜病变（ｄｉａｂｅｔｉｃｒｅｔｉｎｏｐａｔｈｙ，ＤＲ）发生的相关因素，我们对糖尿病患者血浆内皮素－１（ｅｎｄｏｔｈｅｌｉｎ－１，ＥＴ１）进行了检测分析，现报告如下。１对象...     

ET-１ expression and ultrastructural changes inthe retina after exposureto infrasound in rats

to evaluatethe exPressionof ET-1 and ultrastructural changes inthe retinaof SPrague-Dawley rats after exPosureto infrasound. ·METHODS:twenty-five male SPrague-Dawley rats were randomly divided into 5 grouPs, 5 in each grouP, and 4 grouPs were exPosedto infrasoundof 16Hz, 130dB for 2 hours each day, and 1 grouP served as control.the exPosuretime forthe 4 grouPs was resPectively 1, 7, 14 and 21 days.then,the rats were sacrificed after intravenous injection with lanthanum nitrate (La), andthe retina was examined with electron microscoPy and immunochemistry with antibodies against ET-1. ·RESULTS: After infrasonic exPosure for 1 day, ET-1 was exPressed mainly inthe endotheliaof retinal and choroidal blood vessels, so was it inthe control grouP. After infrasonic exPosure for 7 days, it was exPressed mainly inthe retinal Pigment ePithelial cells,outer nuclear layer andouter Plexiformlayer. After exPosure for 14 days, its exPression was enhanced intheouter nuclear layer, inner Plexiform layer and ganglion cell layer. After exPosure for 21 days, its exPression was weakened in all layers. With exPosure goingon,the injury in retina gradually extended fromtheoutertothe inner. Underthe electronic microscoPe, La wasobservedto have infiltrated into several layersofthe retina after 1 dayof exPosure and it became denser and denser fromthe 1sttothe 21st day excePt atthe 7th day. Meanwhile,the retinal layers showed cellular edema, swollenorganelles such as mitochondria and endoPlasmic reticula, karyoPyknosis and edging, cell membrane and karyotheca dilation, ruPture and myelin changes. ·CONCLUSION:the exPressionof ET-1 in retina is relatedtothe locationof infrasonic injury, and ET-1 may have a Protective effecton retina againstthe infrasonic injury.     

神经生长因子对糖尿病大鼠神经视网膜超微结构的影响

目的:通过观测实验性糖尿病动物的神经视网膜的超微结构变化,从视网膜的神经功能角度来探讨糖尿病视网膜病变的发生机制以及相关药物干预后的影响作用。方法:用链脲佐菌素制作糖尿病大鼠动物模型,分为正常对照组(CON组)、糖尿病对照组(DM组)、糖尿病神经生长因子治疗组(D+N组)。分别于病程3,6,9,12mo取大鼠眼球制备石蜡切片,将视网膜组织行HE染色,并将上述标本制备超薄切片,用透射电镜观察并分析。结果:从病程3mo开始,DM组视网膜血管内皮细胞及周细胞的核变形、线粒体肿胀变性、基底膜增厚。视神经节细胞水肿,胞器减少,线粒体变性。光感受器细胞(视锥、视杆)膜盘间隙扩大,线粒体及核也有病理改变。上述病变随病程延长而逐渐加重。经过NGF治疗后,上述DM改变有所减轻,主要表现在感光细胞外节膜盘间隙较DM组缩小,平行度好转;神经细胞突起水肿减轻,胞器水肿好转。各组DM大鼠的视网膜血管、神经网膜及视神经的糖尿病性病变之间未见明显的先后因果关系。结论:神经生长因子对DM大鼠视网膜形态学上所见的视网膜血管、感光细胞和神经节细胞的超微结构改变有着明确的改善作用。在DR的发病过程中,视网膜血管的病变与视网膜神经组织的病变可能是同时存在、互相促进,共同造成糖尿病视网膜病变和视功能的损害。     

高眼压下大鼠视网膜HSP70表达与显微结构变化

目的 研究高眼压下大鼠视网膜热休克蛋白70(HSP70)的表达规律及其高眼压下视网膜电子显微镜下结构变化。方法 本实验分为2部分,第1部分将大鼠右眼制成高眼压模型,维持1h 110mmHg(1mmHg=0.133kPa)高眼压,按观察时间分为4组,每组6只大鼠,分别在4、18、24、48h后摘除眼球,同时每组均有4只大鼠作为对照只灌注,不加压,运用免疫组织化学方法,研究高眼压下大鼠视网膜HSP70的表达规律,第2部分分为免疫组和电镜组,其中免疫组中按高眼压维持时间不同,将动物分为3组,每组6只大鼠,高眼压维持时间分别为:0.5、1.5、2.5h,高眼压去除后,使其生存18h后,摘除眼球,每组也有4只大鼠只灌注不加压。电镜组中动物分组、高压眼作用时间、动物生存时间、对照组设计均与免疫组相一致,其中动物分组均随机分组。结果 高眼压后18h视网膜各层HSP70的表达有显著增高(P<0.01),到24h均有下降,但仍接近18h(细胞内层节段除外)。在本实验的高眼压范围内,电子显微结构变化提示;视网膜视细胞层对高眼压有较强的耐受性,HSP70在此范围高眼压下,视网膜各层内的表达随高眼压作用时间的延长无显著性差异(P>0.05)。结论 高眼压下大鼠视网膜各层HSP70的表达显著增高与视细胞的显微结构变化相一致。     

腺病毒介导睫状神经营养因子在大鼠视网膜中的表达定位

目的观察携带睫状神经营养因子(ciliary neurotrophic factor,CNTF)基因的腺病毒(adenovirus,Ad)载体在正常大鼠视网膜中的表达定位。方法正常成年大鼠40只,随机分为处理组(PBS组、Ad-LacZ组、Ad-CNTF组)及正常对照组,向处理组大鼠眼内分别注射相应溶液,各处理组均分为注射后7d、14d、28d共3个时相点。在相应时相点取大鼠眼球,行冰冻切片,进行免疫组织化学染色。结果Ad-CNTF组各时相点视网膜与其他对照组相比,CNTF阳性染色明显增强,分布更广泛,并且可一直持续到注射后28d。结论Ad-CNTF在正常大鼠眼内注射后,CNTF在视网膜的表达明显增加,且表达时限可达28d。     

Collagen metabolism in the retina of normal and diabetic rats

Glucosyltransferase, an enzyme involved in the synthesis of the carbohydrate portion of basement membranes and collagens, and collagen content were determined in the retina of normal and streptozotocin diabetic rats. No significant difference in glucosyltransferase activity was found at 4 weeks of diabetes. However, the enzyme activity was significantly increased in diabetic rats 12 and 48 weeks following the induction of diabetes. Similarly, a significant increase in collagen content was observed in diabetic retinas after 12 weeks of diabetes. Electron microscopy showed marked thickening of the retinal capillary basement membrane in long-term diabetic (48 weeks) rats. The data suggest that enhanced collagen synthesis and deposition occurs in the retina of diabetic rats, and with duration of diabetes this may result in thickening of the capillary basement membrane. These results are compatible with previously reported increases in kidney glucosyltransferase, collagen synthesis and thickening of the capillary basement membrane in diabetic rats.     

Delayed response of the retina after hyperbaric oxygen exposure

Purpose: To examine retinal electrophysiological function and retinal thickness in healthy eyes before and after hyperbaric oxygen (HBO) exposure. Methods: The healthy eye in each of six subjects who underwent experimental HBO treatment for branch retinal vein occlusion in the fellow eye was examined using multifocal electroretinography (mfERG) and optical coherence tomography (OCT) at baseline and following a course of five consecutive daily sessions of exposure to HBO at 2.4 atmospheres of absolute pressure lasting 90 min each. Results: After HBO, P1 implicit times of the mfERG were significantly shorter than at baseline. The response was delayed, being undetectable on the day treatment concluded, whereas a 2.65% reduction in implicit time was seen 1 week later (p = 0.032). The P1 implicit time remained 2.49% shorter than at baseline 1 month after the end of the HBO sessions (p = 0.020). The bulk of the response to HBO was found in the foveal and parafoveal regions. No detectable change was seen in mfERG amplitudes or in the volume or thickness of the retina. Conclusion:  A mfERG component related to bipolar and Müller cell function was accelerated by a short intermittent exposure to HBO. The response developed after the end of the HBO exposure and lasted for at least 3 weeks, suggesting that it was prompted by the withdrawal of HBO rather than the onset and subsequent brief exposure to HBO.     

A morphological study of the acute toxicity of l-cysteine on the retina of young rats

Systemic administration of l-cysteine to rats (1·2 mg/g body weight) during their first ten days of life leads to a permanent retinal dystrophy which affects the inner layers of retina. To clarify which types of retinal cells that are involved in this lesion, 9- to 10-day-old rats were injected subcutaneously with l-cysteine. The retinas obtained from these animals 4 hr later were examined by light and electron microscopy. Numerous amacrine cells with pyknotic nuclei and swollen cytoplasm were observed. Between these cells undergoing necrosis, well preserved amacrine cells were found. Similar changes were found in about 50% of the ganglion cells. No specific changes were observed in the bipolar cells, the Müller cells or the horizontal cells. The photoreceptors and the pigment epithelium were unaffected. It is concluded that a sublethal dose of l-cysteine given systemically to young rats (up to the age of 10 days), affects subpopulations of the amacrine and the ganglion cells of the retina. Potentially, l-cysteine used in this way, may be a useful scientific tool to destroy selectively populations of retinal neurons.