氧致视网膜血管增殖性病变鼠模型的极简易制备

目的通过极简易的材料及方法建立稳定可靠的视网膜血管增殖性病变动物模型,为进一步探究视网膜血管增殖性疾病的发生机制和治疗方法奠定模型基础。方法使用简单易获取的常用材料,制备简易氧箱。将30只SD新生鼠3窝随机分为模型组(2窝20只)及对照组(1窝10只),模型组于生后第7天置于75%~80%氧浓度箱中饲养5天后返回正常空气中继续饲养,对照组在正常空气中饲养。第17天进行心脏荧光素灌注造影视网膜铺片、眼球连续切片苏木精伊红(HE)染色,以评价模型建立情况。结果自制简易氧箱所建立的模型组新生鼠视网膜血管迂曲扩张,分支血管闭塞,毛细血管无灌注区,血管腊肠样改变,微动脉瘤,新生血管形成;模型组突破视网膜内界膜的血管内皮细胞核数量[(27.3625±3.9562)个/(片.眼)],与对照组[(0.4125±0.6879)个/(片.眼)]比较差异有显著的统计学意义(P<0.01)。结论通过极简易的自制氧箱能有效的建立恒定高氧环境,可为探究视网膜缺血性病变及血管增殖性病变建立稳定、可靠、重复率高的动物模型。     

Recombinant angiostatin prevents retinal neovascularization in a murine proliferative retinopathy model

Retinal neovascularization is central to the pathogenesis of proliferative diabetic retinopathy, the leading cause of blindness among the middle-aged population. Angiostatin, a proteolytic fragment of plasminogen is one of the most promising inhibitors of angiogenesis currently in clinical trials. Here we show that recombinant angiostatin can inhibit retinal neovascularization in a mouse model of proliferative retinopathy. Because proliferative diabetic retinopathy is a recurrent disease, effective therapy will need to be sustained. Recombinant adeno-associated viruses permit long-term expression of transfected genes; however, they can only accommodate a small insert sequence. Thus, we engineered and tested a shortened recombinant angiostatin derivative containing a signal sequence to permit secretion. Recombinant protein was purified from the medium of transfected HEK293 cells and injected subcutaneously into treated animals. The retinal vasculature was analyzed in retinal flat mounts and using immunohistochemically stained sections. Both methods demonstrate that this short, secreted form of angiostatin is effective in reducing the development of blood vessels in a nontumor environment and has therapeutic potential for neovascular retinopathies such as diabetic retinopathy, retinopathy of prematurity, retinal vein occlusion and, possibly, age-related macular degeneration.     

早产儿视网膜病的早期护理干预

新生儿易引起低钙血症，而出现惊厥或其他明显神经肌肉兴奋症状，一般给予补充钙剂。葡萄糖酸钙静脉注射纠正新生儿低钙血症疗效迅速且显著，因此在新生儿科应用较多。葡萄糖酸钙具有强烈的刺激性，外渗可使局部组织变性、坏死。现将我科2例静脉注射10％葡萄糖酸钙后致软组织钙化情况报告如下。     

早产儿视网膜病的早期护理干预

随着医学的发展和NICU抢救水平的提高,早产儿存活率逐年上升。随着早产儿存活率的升高,早产儿视网膜病(ROP)也相应增加。2004年10月—2005年3月我科收住60例ROP早产儿。现将护理报告如下。1临床资料本组男37例,女23例。孕26周~36周,胎龄(32.0±2.3)周,体重0.9kg~2.5kg(1.48kg±0.46kg)。其中入院时诊断为超低出生体重儿1例,极低出生体重儿19例,缺血缺氧性脑病20例,肺透明膜病17例,胎粪吸入性肺炎3例。2护理2.1合理用氧早产是发生ROP的主要原因,高浓度氧可诱发ROP。早产低体重由于呼吸系统发育不成熟,通气和换气功能障碍,生后给予一定…     

多生子早产儿视网膜病变的临床特点

目的 观察多生子早产儿视网膜病变(ROP)的发生发展特点,探讨影响ROP发生发展的相关因素.方法 对湖南省儿童医院新生儿科及眼科2006年4月至如11年4月收治的胎龄<35周,体重<2000 g的早产儿在出生后2周开始采用间接眼底镜及巩膜压迫器观察视网膜.根据早产儿视网膜病变国际分类法分期记录ROP病变,同时记录患儿全身疾病并发情况,观察及分析多生子与单生子中ROP发生的临床特点及相关因素.结果 共筛查33049例胎龄<35周,体重<2000 g的早产儿,其中单生子25082例,双生子7934例,三生子33例;男21179例,女11870例;结果 发现多生子ROP的发病率高于单生子(P<0.05);多生子组中低胎龄、低体重儿及颅内出血、贫血、窒息等疾病发生率高(P<0.05);多胎ROP发生更严重(P<0.05).结论 由于多生子出生体重轻、胎龄低及常合全身并发症,故ROP的发病率高于单生子,且发病早,病情相对严重.     

早产儿视网膜病变的原因及护理干预

介绍了早产儿视网膜病变(ROP)的主要病因,认为早产、低出生体重是ROP的根本原因,氧疗与ROP密切相关,其危害程度主要取决于吸入氧浓度、用氧持续时间和用氧方式,并提出了具体的护理干预措施。     

早产儿视网膜病危险因素分析

目的调查瑞安市人民医院早产儿视网膜病（ROP）的发生率和高危因素。方法2005年8月1日至2008年8月1日对瑞安市人民医院新生儿监护病房（NICU）住院并符合筛查标准的540例新生儿进行了ROP筛查。结果在接受筛查的540例新生儿中,44例发生了ROP,发生率为8.1%。Ⅰ～Ⅲ期病变分别为35、7、和2例;其中2例需激光治疗,无失明病例。结论ROP相关因素的logistic回归分析结果表明,孕周、出生体重、吸氧时间、呼吸窘迫综合征是ROP形成的高危因素。     

早产儿视网膜病变的原因及护理干预

介绍了早产儿视网膜病变（ROP）的主要病因，认为早产、低出生体重是ROP的根本原因，氧疗与ROP密切相关。其危害程度主要取决于吸入氧浓度、用氧持续时间和用氧方式，并提出了具体的护理干预措施。     

6例早产儿视网膜病变的护理

早产儿视网膜病变(retinopathy of prematurity,ROP),是早产、低体重儿发生的一种视网膜毛细血管发育异常的双侧眼病。根据病变的严重程度ROP可分5期:1期或2期仅需临床观察,对于阈值病变3期应尽早行激光治疗;病变进展到4期或5期后,即使手术成功也只能使患儿保留光感或较低视力[     

Selective blockade by nicergoline of vascular responses elicited by stimulation of alpha 1A-adrenoceptor subtype in the rat

The alpha 1-adrenergic blocking activity of nicergoline was re-examined in rats, with a particular emphasis on alpha 1-adrenoceptor subtypes. In pithed rats, nicergoline and prazosin infused at a single small dose (0.5 microgram/kg/min i.v.) produced a substantial and identical shift to the right of the control dose pressor response curve to the specific alpha 1-agonist cirazoline (ED50 = 4.0 +/- 0.1, 4.0 +/- 0.1 and 0.9 +/- 0.01 microgram/kg i.v. for nicergoline, prazosin and vehicle respectively). In the isolated perfused mesenteric vascular bed, nicergoline strongly inhibited the pressor responses elicited by cirazoline, with approximately 40-fold higher potency (pA2 = 11.1 +/- 0.3) than prazosin (pA2 = 9.5 +/- 0.3). Conversely, nicergoline was 20-fold less potent than prazosin to antagonize the contractile effects of cirazoline in isolated endothelium-denuded aorta (pA2 = 8.6 +/- 0.2 and 9.9 +/- 0.2 for nicergoline and prazosin respectively). Pretreatment of mesenteric vascular beds with chloroethylclonidine did not significantly modify nicergoline antagonistic potency (pA2 = 10.6 +/- 0.2). Nicergoline displaced [3H]-prazosin bound to rat forebrain membranes pretreated with chloroethylclonidine (pKi = 9.9 +/- 0.2) at concentrations 60-fold lower than in rat liver membranes (pKi = 8.1 +/- 0.2). Finally, of the nicergoline metabolites studied, lumilysergol acted as a modest alpha 1 antagonist (bromonicotinic acid was devoid of alpha 1 antagonist activity). In conclusion, nicergoline is a potent and selective alpha 1A-adrenoceptor subtype antagonist, an alpha 1-adrenoceptor subtype which is mainly represented in resistance arteries.     

小鼠氧诱导视网膜新生血管形成中EphA2与VEGF的表达及相关性研究

目的探讨促红细胞生成素产生肝细胞受体A2(Eph A2)与血管内皮生长因子(VEGF)在C57BL/6小鼠氧诱导视网膜新生血管病变模型(OIR)中的表达以及相关性。方法新生C57BL/6小鼠120只,随机分为实验组和对照组,每组各60只。实验组小鼠建立OIR模型,对照组饲养于正常氧环境。各组小鼠于出生后第17天处死,将小鼠眼球行组织切片后HE染色,计数突破视网膜内界膜新生血管内皮细胞核数。放射免疫法检测小鼠视网膜组织Eph A2和免疫组织化学染色检测视网膜VEGF含量,分析二者的相关性及与视网膜新生血管的关系。结果实验组视网膜大量新生血管形成,实验组小鼠视网膜切片新生血管细胞核计数明显高于对照组(99.10±3.15/个比4.20±0.89/个),差异有统计学意义(t=28.53,P0.01)。各组视网膜中Eph A2的ELISA检测结果:实验组Eph A2含量明显高于对照组(80.82±20.70 pg/ml比14.42±6.80 pg/ml),差异有统计学意义(t=23.23,P0.01)。视网膜免疫组织化学染色显示,VEGF实验组视网膜组中表达明显升高,在对照组小鼠视网膜有微弱表达,实验组VEGF吸光度值高于对照组(5.19±0.75比1.88±0.33),差异有统计学意义(t=13.42,P0.05)。Eph A2和VEGF两者的表达显著相关(r=0.85,P0.05)。结论 Eph A2与VEGF的表达在小鼠视网膜新生血管形成中呈正相关,提示两者可能存在协同效应。     

Cryotherapy: a new treatment for retinopathy of prematurity

More than 2,600 infants have some degree of eye damage and loss of vision from retinopathy of prematurity (ROP) each year in the United States. Transcleral cryotherapy, a treatment that has been shown to decrease vision loss due to ROP by 50%, is now being used in the United States.     

Genetic causes of retinal degeneration

Premature death of rod and cone photoreceptor cells in the human retina leads to severe visual handicaps in affected patients. The two most important groups of retinal dystrophies, macular degeneration and retinitis pigmentosa, differ in primary symptoms and disease progression. Macular degeneration starts in the central retina and progresses towards the periphery. In RP, photoreceptor cell death starts in the periphery and then proceeds to the central part of the retina. Molecular studies have revealed important new findings during the last decade. There are two important results to be emphasized: 1. The very same clinical symptoms can result from mutations in different genes. RP is a prominent example for this phenomenon. 2. Mutations in the same gene can result in different phenotypes. The correlation between genotype and phenotype is not essentially straight forward. This may indicate that other factors can influence the phenotypic consequences of mutations. Different X-linked retinal dystrophies represent excellent examples for these findings.     

β-secretase 1 overexpression by AAV-mediated gene delivery prevents retina degeneration in a mouse model of age-related macular degeneration

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von Willebrand factor and retinal circulation in early-stage retinopathy of type 1 diabetes

OBJECTIVE: Although retinopathy is a common microvascular complication of type 1 diabetes, the mechanism for this complication is still unknown. Changes in retinal circulation have been noted before the development of overt retinal pathology. Because von Willebrand factor (vWF) is a marker for endothelial dysfunction and mediates platelet adhesion, we determined if there was an association between vWF and retinal circulation in the early stages of diabetic retinopathy. RESEARCH DESIGN AND METHODS: Twenty subjects (aged 32.4 +/- 7.8 years) with type 1 diabetes and minimal or no retinopathy were studied. The mean duration of diabetes was 4.7 +/- 2.6 years. Data were collected at baseline and after 4 months of 1,800 IU vitamin E therapy or placebo. Retinal circulation was evaluated by video fluorescein angiography. Plasma vWF antigen levels were measured by enzyme-linked immunosorbent assay and fibrinogen by the Clauss method. RESULTS: Retinal blood flow was negatively correlated with vWF levels (r = -0.44, P = 0.008), whereas retinal circulation time was positively correlated with vWF levels (r = 0.33, P = 0.048). Fibrinogen levels were not significantly associated with either retinal index. However, fibrinogen levels were positively associated with HbA1c levels (r = 0.34, P = 0.01), indicating an association between poor glycemic control and higher fibrinogen levels. CONCLUSIONS: Increased vWF was associated with a prolonged retinal circulation time and reduced retinal blood flow in early-stage retinopathy of type 1 diabetes. Reduced blood flow associated with increased vWF levels may promote stasis in the retinal circulation and lead to local hypoxemia. These changes might contribute to the microvascular complications of diabetes. Whether the vWF levels predict retinal complications deserves further investigation.     

糖尿病视网膜病变的MR研究进展

视网膜是体内代谢最旺盛的组织器官之一,氧需求量很高.视网膜长期处于低氧状态(如糖尿病眼病)会产生显著的、严重的不良后果,一般认为这是导致视网膜结构或功能不可逆性改变的根本原因.然而,采用传统方法测量视网膜氧张量有多方面的局限性.随着磁共振成像技术的发展,采用MRI进行无创地检测视网膜氧张量变化已成为可能.本文对糖尿病视网膜病变的MR研究进展进行综述.