糖尿病患者视网膜前新生血管膜中血管内皮细胞的增殖和激活

目的 研究Ⅰ型糖尿病患者增殖型糖尿病视网膜病变(proliferative diabetic retinopathy,PDR)视网膜前新生血管膜中血管内皮细胞的增殖和激活状态。 方法用双重免疫荧光及碱性磷酸酶抗碱性磷酸酶法检查Ⅰ型糖尿病患者18例PDR视网膜前新生血管膜血管内皮细胞的增殖和激活状态，并与患者的主要临床特征相比较。 结果 18例标本中,16例(88.9%)含增殖状态的血管内皮细胞，14例(77.8%)的内皮细胞呈激活状态;应用双重染色技术,发现在含增殖状态内皮细胞的16例中有14例(87.5%)内皮细胞同时处于激活状态。 结论 PDR视网膜前新生血管膜中大多数新生血管内皮细胞呈增殖和激活状态，提示血管内皮细胞在PDR的病理生理和发展中起重要作用。(中华眼底病杂志,1998,14:141-143)     

氩激光视网膜光凝治疗增殖型糖尿病视网膜病变的疗效

对增殖性糖尿病视网膜病变(proliferative diabetic retinopathy,PDR)患者270例363眼氩激光视网膜光凝疗效进行分析。光凝后新生血管消退、未再玻璃体出血者占63.6%，其中视网膜新生血管与视盘新生血管、视网膜新生血管合并视盘新生血管间疗效差异均非常显著(P<0.01)；单纯新生血管与新生血管合并玻璃体出血行间疗效差异非常显著(P<0.01)。表明氩激光视网膜光凝治疗增殖性糖尿病视网膜病变的疗效与新生血管的存在部位及是否合并玻璃体出血有关。 （中华眼底病杂志，1995，11：227-228）     

血管内皮细胞生长因子在糖尿病性视网膜病变进展中的作用

糖尿病性视网膜病变是糖尿病微血管病变常见而严重的并发症,在很大程度上导致不可逆的视功能损害或完全失明.VEGF在DR发生、发展,尤其在视网膜新生血管形成过程中发挥重要作用,本文就血管内皮生长因子与糖尿病性视网膜病变的关系进行综述。     

视网膜新生血管的药物治疗研究进展

全身或局部的病变可导致血—视网膜屏障破坏、血液微循环障碍和血管通透性改变,进一步引起视网膜缺氧,乃至水肿,随之视网膜组织对缺氧发生一系列代偿性反应,在各种细胞因子、细胞内外调控机制的共同作用下生成新生血管,目的是补偿缺血缺氧的视网膜。视网膜新生血管相关疾病包括糖尿病性视网膜病变、视网膜静脉周围炎、早产儿视网膜病变等。抑制新生血管生长是治疗这类疾病的关键。本文对抑制视网膜新生血管药物的研究进展作一综述。     

血管生成促进因子在糖尿病视网膜病变新生血管形成中的作用

糖尿病视网膜病变(diabetic retinopathy,DR)是糖尿病最常见和最严重的并发症之一.目前,DR的发病机制尚不明确,但近年来研究表明,血管生成促进因子与DR新生血管的发生、发展密切相关,是导致视网膜新生血管形成的主要致病因子.本文就血管生成促进因子在DR新生血管形成中的作用进行综述.     

视网膜血管搭桥术

视网膜中央动脉为终末动脉 ,它的阻塞可引起视网膜急性缺血 ,极短时间内可导致视功能严重损害 ;视网膜中央静脉阻塞远较视网膜中央动脉阻塞常见 ,视功能损害亦相当严重 ,甚至因新生血管性青光眼而失明。欧美国家最常见的视网膜血管疾病中 ,视网膜中央静脉阻塞是第 2位 ,仅次于糖尿病性视网膜病变。视网膜血管无论是动脉还是静脉均缺乏吻合支 ,阻塞后的血液循环不易改善 ,这一特点与心脏冠状血管系统有相似之处。在心脏科领域 ,冠状血管搭桥术是治疗心肌缺血的有效方法 ,那么在眼部是否能通过血管搭桥手术来解决视网膜血管性疾病呢 ?本文就视…     

增殖期糖尿病视网膜病变伴牵拉性视网膜脱离患者新生血管膜分布特点的临床研究

目的 探讨增殖期糖尿病视网膜病变(PDR)伴牵拉性视网膜脱离的患者新生血管膜分布及粘连特点.方法 本研究收集2015年11月-2017年01月于安徽省立医院眼科住院诊断增殖期糖尿病视网膜病变(PDR)合并牵拉性视网膜脱离明确的54例54只眼.于玻切手术术中,根据视盘部是否覆盖新生血管膜、临床分区、象限分区三个指标分别记录新生血管膜位置.记录新生血管膜面积、新生血管膜在视盘部及眼底象限分区有无粘连.记录随访至术后6个月的术眼的最佳矫正视力(BCVA)及网膜复位情况.结果 视盘部新生血管膜发病率约为72.2％.按照临床分区,新生血管膜的分布为后极部分布较多,占70.4％.按照象限分区,新生血管膜在鼻上方、鼻下方分布较多,分别为57.4％和55.6％.在合并有视盘部新生血管膜39例39眼中,与视盘部有粘连占30.8％.新生血管膜粘连在鼻上方及鼻下方较多,分别为55.6％和50.0％.随访至术后6个月,术后平均BCVA较术前平均BCVA提高,差异具有统计学意义(Z=-5.470,P＜0.05).视网膜复位率是87.0％.结论 糖尿病视网膜病变(DR)患者中,合并视盘部新生血管膜发病率高.新生血管膜大部分集中在视网膜后部眼底及鼻侧.新生血管膜主要在鼻侧、视盘部粘连较多且牢固,粘连一般位于视网膜血管处.玻切手术可以改善患者的视力预后,网膜复位率也可以达到87.0％.     

糖尿病视网膜病变的新生血管生长方式及细胞成分的研究进展

增生性糖尿病视网膜病变(PDR)是糖尿病严重并发症之一,不及时治疗常导致失明.新生血管的产生是PDR的特征性表现,也是导致视力下降的主要病理变化.及时抑制视网膜新生血管的产生,可以有效降低PDR造成的病理损害.目前对PDR中新生血管的产生机制尚未明了.本文就PDR病变中新生血管的生长方式及参与作用的细胞成分作一综述.     

全视网膜光凝治疗糖尿病视网膜病变的重复应用指征

目的:探讨重复应用全视网膜光凝治疗糖尿病视网膜病变的指征。方法:糖尿病视网膜病变患者122例(212眼),78例(126眼)为非增生期,44例(86眼)为增生期。采用ND-YAG氩绿激光(波长530nm)进行全视网膜光凝,治疗分3~4期进行。术后24~36mo随访,评价视力变化、视网膜病变进展和视网膜新生血管消退情况。结果:治疗后视力(0.3的患者量明显小于治疗前,继续下降比率明显减少;全视网膜光凝术后3,12,24mo和36mo视网膜病变稳定率分别为73.6%,80.0%,84.0%,85.4%;新生血管消退分别达到38.6%,56.2%,73.6%,81.4%,治疗后视网膜新生血管逐渐减少。结论:如果存在严重视网膜缺氧征象,即出现小动脉瘤、微小出血点积聚、严重的视网膜内微血管异常和小静脉明显形成时,可多次重复应用全视网膜光凝治疗糖尿病视网膜病变。     

氪激光治疗视盘新生血管型糖尿病视网膜病变的疗效观察

目的探讨氪激光治疗视盘新生血管型糖尿病视网膜病变的疗效。方法对20例(25只眼)视盘新生血管型糖尿病视网膜病变患者使用氪激光行超全视网膜光凝治疔。光凝术后3、6、12个月分别行荧光素眼底血管造影检查,新生血管如未完全消退则追加光凝。随访3～20个月(平均9.5个月)。结果超全视网膜光凝术后视力提高者12只眼(48.0%),视力不变者12只眼(48.0%),视力下降者1只眼(2.0%);19只眼(76.0%)新生血管消退或部分消退,6只眼(24.0%)新生血管无变化或加重。16只眼(61.5%)需要补充光凝。平均激光量为2600点。结论视盘新生血管型糖尿病视网膜病变较常规治疗需要更大的激光量,光凝术后应定期随访观察,必要时补充光凝。     

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.