糖尿病视网膜病变激光光凝术后的超声生物显微镜检测

糖尿病视网膜病变(diabetic retinopathy，DR)的视网膜激光光凝主要用于治疗严重非增生性DR、增生性DR和具有临床意义的黄斑水肿(clinically significant macular edema)，视网膜激光光凝有助于保存原有视力。但视网膜激光光凝引起的眼部并发症不容忽视。我们应用超声生物显微镜(ultrasound biomicroscopy，UBM)对22例DR患者的33只眼视网膜激光光凝术前、后眼前段改变进行了检测，现将结果报道如下。     

糖尿病视网膜病变激光治疗的时机与方法

1970年Beetham和Aiello以红宝石激光对增生性糖尿病视网膜病变（proliferative diabetic retinopathy，PDR）的周边眼底进行光凝治疗获得成功，为播散性视网膜光凝治疗糖尿病视网膜病变（diabetic retinopathy，DR）奠定了基础。目前，视网膜激光光凝已成为全世界公认的治疗DR的主要方法。     

糖尿病视网膜病变不同分期的激光光凝治疗

中国约有5％的糖尿病患者发生糖尿病视网膜病变（diabetic retinopathy，DR），约5％发生增生型DR（proliferative DR，PDR），及时的视网膜广泛光凝可以延缓晚期并发症的发生。本研究对不同分期的DR进行视网膜光凝治疗，观察临床疗效。     

糖尿病视网膜病变激光治疗的并发症及其防治

糖尿病视网膜病变是慢性高血糖造成的慢性缺血性视网膜病变,是糖尿病微血管并发症之一,可严重影响患者视力甚至致盲。DR致盲的主要原因包括黄斑水肿、玻璃体积血以及新生血管性青光眼等,视网膜激光光凝是目前临床上治疗DR的最主要方法之一。其原理是利用激光的热效应,使蛋白质变性,组织凝固、破坏并结痂。使耗氧低的瘢痕组织代替耗氧高的视锥、视杆细胞,减少组织耗氧,改善中周部视网膜缺血缺氧状态。但激光治疗的过程中可能会出现黄斑水肿、玻璃体积血、视野缺损等并发症,为了更全面地评估激光治疗的益处和风险,本文就近几年来有关DR激光治疗的并发症及其防治方法的文献进行综述。     

视杆细胞与视网膜新生血管

视网膜新生血管是糖尿病视网膜病变和早产儿视网膜病变的重要病理特征，其形成与视网膜局部缺血缺氧有关。研究显示视杆细胞代谢消耗大量氧，可致局部缺氧，与视网膜新生血管形成可能有关。而光照抑制视杆细胞代谢可减少氧消耗，对抑制以上疾病新生血管的形成可能有效。（中华眼底病杂志，2007，23：152-154）     

糖尿病视网膜病变患者白内障术后低视力的光凝治疗

目的 评价视网膜光凝对糖尿病视网膜病变（DR）患者白内障手术后低视力的治疗效果.方法 回顾性分析白内障术后低视力的DR 52例（52眼）,根据治疗方法不同分为两组：接受视网膜光凝治疗的26例,为A组;未接受视网膜光凝治疗的26例,为B组.比较两组患者在白内障术后3个月、6个月时的最佳矫正视力（BCVA）和低视力眼数.结果 白内障术后3个月时,两组BCVA差异无统计学意义（P＞0.05）;术后6个月时,两组BCVA差异有统计学意义（P＜0.05）,A组优于B组.A组有低视力15例（57.69％）,B组有21例（80.77％）.A组有1例（3.85％） DR病情发展,B组有7例（26.92％）.结论 视网膜光凝可以改善DR患者白内障术后低视力的状态,控制DR病情.     

糖尿病视网膜病变全视网膜激光光凝前后视网膜中央动静脉多普勒超声血流变化

激光光凝是目前治疗糖尿病视网膜病变（DR）的有效方法之一，激光光凝后，视网膜微循环受到影响，作为构成视网膜内层微循环主要血管的视网膜中央动脉（CRA）和视网膜中央静脉（CRV）激光光凝后血流动力学变化的客观检查报道不多，我们利用彩色超声多普勒（CDFI）对一组DR患者全视网膜激光光凝（PRP）前后的CRA、CRV血流动力学指标进行了检测，现将结果报道如下。     

视网膜激光治疗糖尿病性视网膜病变的临床观察

目的观察倍频532nm激光视网膜光凝术治疗糖尿病性视网膜病（DR）的疗效。方法用倍频532nm激光对298例（568只眼）增生前期和增生早期DR患者进行视网膜光凝治疗。光凝3～6次,术后平均随访9个月。结果治疗后182只眼（32%）视力提高,视力无变化352只眼（62%）,视力下降34只眼（6%）。随病变程度增加疗效降低（P〈0.01）。荧光素眼底血管造影（FFA）及相干光断层扫描（OCT）检查,有黄斑水肿的272只眼中,光凝后水肿完全消退者142只眼（52%）,部分消退者122只眼（45%）,不变者82只眼（3%）。结论倍频532nm激光视网膜光凝术治疗DR有效,在增生前期治疗效果好。     

视杆细胞视觉传导的慢快通道及临床应用研究进展

视杆细胞对视觉,特别是暗视觉的形成具有重要的作用。视杆细胞与神经节细胞之间视觉传导的具体通道和过程目前尚不清楚。20年前,国外学者认识到在视网膜视杆细胞与神经节细胞之间的视觉传导可能并非只存在一条通道。在15Hz频率下,利用暗适应闪烁光视网膜电图（ERG）可将视杆细胞慢快通道的各自反应分离出来。某些疾病,如视网膜色素变性（RP）、Stargardt黄斑营养不良、完全性静止性夜盲的暗适应15Hz闪烁光ERG反应则表现出某些特性。就视杆细胞多条视觉传导通道的发现、传导途径及临床应用进行综述。     

新的光凝方式对视力较好的糖尿病视网膜病变的疗效观察

目的评估一种新的光凝方式（少量分区法）对视力较好的糖尿病性视网膜病变（DR）患者治疗后视力的变化和疗效分析。方法荧光素眼底血管造影（FFA）确诊为增生前期及增生期的DR患者19例（28只眼）,视力0.8以上,糖化血红蛋白低于6.5%,根据FFA和相干光断层扫描（OCT）的结果分次行视网膜光凝,每次光凝间隔时间1～6周,每次光凝点数不超过300点,首次黄斑区光凝,不超过200点。观察治疗前后视力的变化及视网膜增生情况的变化。结果视网膜光凝结束后随访观察1个月,视力提高和保持不变27只眼,占96.4%,仅1只眼视力下降至0.5。增生性糖尿病性视网膜病变眼视网膜新生血管消退。结论减少每次光凝点数,增加光凝次数,增大光凝间隔时间对保持DR光凝后视力的稳定有良好的效果。     

Photoreceptor cells and RPE contribute to the development of diabetic retinopathy

Diabetic retinopathy (DR) is a leading cause of blindness. It has long been regarded as vascular disease, but work in the past years has shown abnormalities also in the neural retina. Unfortunately, research on the vascular and neural abnormalities have remained largely separate, instead of being integrated into a comprehensive view of DR that includes both the neural and vascular components. Recent evidence suggests that the most predominant neural cell in the retina (photoreceptors) and the adjacent retinal pigment epithelium (RPE) play an important role in the development of vascular lesions characteristic of DR. This review summarizes evidence that the outer retina is altered in diabetes, and that photoreceptors and RPE contribute to retinal vascular alterations in the early stages of the retinopathy. The possible molecular mechanisms by which cells of the outer retina might contribute to retinal vascular damage in diabetes also are discussed. Diabetes-induced alterations in the outer retina represent a novel therapeutic target to inhibit DR.     

Cellular remodeling in mammalian retina: results from studies of experimental retinal detachment

Retinal detachment, the separation of the neural retina from the retinal pigmented epithelium, starts a cascade of events that results in cellular changes throughout the retina. While the degeneration of the light sensitive photoreceptor outer segments is clearly an important event, there are many other cellular changes that have the potential to significantly effect the return of vision after successful reattachment. Using animal models of detachment and reattachment we have identified many cellular changes that result in significant remodeling of the retinal tissue. These changes range from the retraction of axons by rod photoreceptors to the growth of neurites into the subretinal space and vitreous by horizontal and ganglion cells. Some neurite outgrowths, as in the case of rod bipolar cells, appear to be directed towards their normal presynaptic target. Horizontal cells may produce some directed neurites as well as extensive outgrowths that have no apparent target. A subset of reactive ganglion cells all fall into the latter category. Muller cells, the radial glia of the retina, undergo numerous changes ranging from proliferation to a wholesale structural reorganization as they grow into the subretinal space (after detachment) or vitreous after reattachment. In a few cases have we been able to identify molecular changes that correlate with the structural remodeling. Similar changes to those observed in the animal models have now been observed in human tissue samples, leading us to conclude that this research may help us understand the imperfect return of vision occurring after successful reattachment surgery. The mammalian retina clearly has a vast repertoire of cellular responses to injury, understanding these may help us improve upon current therapies or devise new therapies for blinding conditions.     

昼夜节律和生物钟基因与糖尿病视网膜病变发病的相关性研究进展

糖尿病视网膜病变(diabetic retinopathy, DR)是糖尿病患者最常见的微血管并发症,已成为全球工作年龄人群视力障碍的主要原因之一。DR的发生是多种机制共同作用的结果,越来越多的研究表明昼夜节律及生物钟基因与DR的发病密切相关。昼夜节律是受生物钟基因调控,以24h为周期,与外界明暗变化相一致的生理过程,生物钟调控机体的各种生理活动。昼夜节律紊乱通过影响糖尿病患者的血糖水平和眼部的生理稳态等诱导DR的发生,生物钟基因可能通过调控DR的氧化应激反应、炎症反应、视网膜自噬节律、线粒体功能障碍以及内皮祖细胞功能等各方面参与DR的发病。本文介绍了昼夜节律的产生及调控机制,以及视网膜内在昼夜节律生物钟,深入探讨了昼夜节律系统以及生物钟基因在DR发生发展过程中的影响,旨在为DR的预防及治疗提供参考。     

Novel approaches for treating diabetic retinopathy based on recent pathogenic evidence

Diabetic retinopathy remains as a leading cause of blindness in developed countries. Current treatments target late stages of DR when vision has already been significantly affected. A better understanding of the pathogenesis of DR would permit the development of more efficient preventional/interventional strategies against early stages of DR. In this article a critical review of the state of the art of this issue is provided along with a discussion of problems which have yet to be overcome. Neuroprotection as a new approach for the treatment of the early stages of DR has been particularly emphasized.The development and progression of DR is not homogeneous and, apart from blood glucose levels and blood pressure, it depends on genetic factors which remain to be elucidated. In addition, the role of the pathogenic pathways is not the same in all patients. All these factors should be taken into account in the near future when an individualized oriented treatment for DR could become feasible. The new techniques in retinal imaging acquisition, the identification of useful circulating biomarkers and the individualized analysis of biological samples could facilitate the development of early and personalized therapy in the setting of DR.Finally, it should be noted that only a coordinated action among ophthalmologists, diabetologists, basic researchers, experts in pharmaco-economics and health care providers addressed to the design of rational strategies targeting prevention and the early stages of DR will be effective in reducing the burden and improving the clinical outcome of this devastating complication of diabetes.     

Characterization of the rod photoresponse isolated from the dark-adapted primate ERG

The a-wave of the human dark-adapted ERG is thought to derive from activity of rod photoreceptors. However, other sources within the retina could potentially perturb this simple equation. We investigated the extent to which the short-latency dark-adapted rod a-wave of the primate ERG is dominated by the rod photoresponse and the applicability of the phototransduction model to fit the rod a-wave. Dark-adapted Ganzfeld ERGs were elicited over a 5-log-unit intensity range using short bright xenon flashes, and the light-adapted cone responses were subtracted to isolate the rod ERG a-wave. Intravitreal 4-phosphono-butyric acid (APB) and cis-2,3-piperidine-dicarboxylic acid (PDA) were applied to isolate the photoreceptor response. The Hood and Birch version of the phototransduction model, Rmax[1 - e(-I x S x (t-t(eff)))2], was fitted to the a-wave data while allowing Rmax and S to vary. Three principle observations were made: (1) At flash intensities > or =0.77 log sc-td-s the leading edge of the normalized rod ERG a-wave tracks the isolated photoreceptor response across the first 20 ms or up to the point of b-wave intrusion. The rod ERG a-wave was essentially identical to the isolated receptor response for all intensities that produce peak responses within 14 ms after the flash. (2) The best fit of sensitivity (S) was not affected by APB and/or PDA, suggesting that the inner retina contributes very little to the dark-adapted a-wave. (3) APB always reduced the maximum dark-adapted a-wave amplitude (by 15-30%), and PDA always increased it (by 7-15%). Using the phototransduction model, both events can be interpreted as a scaling of the photoreceptor dark current. This suggests that activity of postreceptor cells somehow influences the rod dark current, possibly by feedback through horizontal cells (although currently not demonstrated for the rod system), or by altering the ionic concentrations near the photoreceptors, or by neuromodulator effects mediated by dopamine or melatonin.     

Spatial summation properties of goldfish ganglion cells.

At threshold the eye is known to sum quanta as though the total catch were important and not the distribution on the retina. In humans, spatial summation is larger under dark adapted conditions. The extent of this spatial summation is studied in goldfish retinal ganglion cells which are known to receive both rod and cone inputs. The area of summation in single ganglion cells is found to be much larger for rod input compared to cone input. It seems that in single ganglion cells, the spatial summating properties increase markedly in the dark due largely to the neural organization of rod and cone input.     

中药单体治疗糖尿病视网膜病变的研究进展

糖尿病视网膜病变(DR)是一种常见的糖尿病慢性并发症,可导致视网膜中微血管的不可逆性损伤,是糖尿病患者首要致盲性眼病。DR的发病机制主要涉及氧化应激、炎症反应与新生血管形成等因素。临床上多以视网膜激光光凝术、玻璃体切割术或药物治疗为主。我国传统中药组方与中药单体在DR治疗,特别是视网膜保护方面具有独特功效,为DR治疗提供有益补充。本文综述了代表性中药组方与中药单体在DR治疗中的应用实践与作用机制,以期为DR的临床治疗与新药研发提供参考。     

The rod circuit in the rabbit retina

Mammalian retinae have a well-defined neuronal pathway that serves rod vision. In rabbit retina, the different populations of interneurons in the rod pathway can be selectively labeled, either separately or in combination. The rod bipolar cells show protein kinase C immunoreactivity; the rod (AII) amacrine cells can be distinguished in nuclear-yellow labeled retina; the rod reciprocal (S1 & S2) amacrine cells accumulate serotonin; and the dopaminergic amacrine cells show tyrosine-hydroxylase immunoreactivity. Furthermore, intracellular dye injection of the microscopically identified interneurons enables whole-population and single-cell studies to be combined in the same tissue. Using this approach, we have been able to analyze systematically the neuronal architecture of the rod circuit across the rabbit retina and compare its organization with that of the rod circuit in central cat retina. In rabbit retina, the rod interneurons are not organized in a uniform neuronal module that is simply scaled up from central to peripheral retina. Moreover, peripheral fields in superior and inferior retina that have equivalent densities of each neuronal type show markedly different rod bipolar to AII amacrine convergence ratios, with the result that many more rod photoreceptors converge on an AII amacrine cell in superior retina. In rabbit retina, much of the convergence in the rod circuit occurs in the outer retina whereas, in central cat retina, it is more evenly distributed between the inner and outer retina.     

The pathogenesis of early retinal changes of diabetic retinopathy

Recent successful trials of antibodies to vascular endothelial growth factor (VEGF) in diabetic retinopathy implicate this cytokine as a major cause of diabetic retinopathy (DR) and diabetic macular oedema (DME). The mechanisms which cause VEGF to be over-expressed to cause the vasculopathy are not entirely clear. This review explores the earliest changes to the retina in DR and the factors that predispose or prevent DR, including sleep apnoea, receptor degenerations laser treatment and VEGF polymorphism. The review also presents the evidence that retinal hypoxia, existing in the earliest stages, causes DR. This hypoxia is much increased by dark adaptation, indicating a new and possibly superior therapy.     

Role of inflammatory cells in pathophysiology and management of diabetic retinopathy

Diabetic retinopathy (DR) is a sight-threatening complication of diabetes mellitus. Several inflammatory cells and proteins, including macrophages and microglia, cytokines, and vascular endothelial growth factors, are found to play a significant role in the development and progression of DR. Inflammatory cells play a significant role in the earliest changes seen in DR including the breakdown of the blood retinal barrier leading to leakage of blood into the retina. They also have an important role in the pathogenesis of more advanced stage of proliferative diabetic retinopathy, leading to neovascularization, vitreous hemorrhage, and tractional retinal detachment. In this review, we examine the function of numerous inflammatory cells involved in the pathogenesis, progression, and role as a potential therapeutic target in DR. Additionally, we explore the role of inflammation following treatment of DR.