神经生长因子巩膜外缓释给药的研究

目的探讨巩膜外植入神经生长因子(NGF)药膜后其眼内的药代动力学改变,研究该药膜是否有缓释效果,改善NGF给药途径。方法筛选与NGF有亲和力的胶原组织,制成具有单向缓释功能的药膜,将其植入健康白兔巩膜表面,用ELISA法测定并观察对照组和实验组各时间点玻璃体内NGF质量浓度的变化,用3P97药代动力学程序计算主要药代动力学参数。结果实验组在药膜植入后2~15d内NGF质量浓度明显高于对照组,第18d降至正常。第3d达到峰质量浓度20·91ng/ml,半衰期约7·41d。药-时曲线下面积AUC0-18为232·78801ng·d/ml。结论自制NGF药膜可缓释进入玻璃体,其峰浓度较高,消除半衰期较长,质量浓度波动较小。     

蛇毒神经生长因子在兔眼内的药代动力学研究

目的　研究蛇毒神经生长因子 (venomnervegrowthfactor ,v_NGF)兔眼结膜下及玻璃体内注射两种给药方式 ,不同时间内玻璃体中的药代动力学行为。方法　蛇毒神经生长因子经13 1I标记 ,在注射入兔眼结膜下和玻璃体腔后测定玻璃体内 1h、3h、6h、12h、2 4h、48h的13 1I每分钟计数率 (CPM)。结果　经分析表明 ,结膜下注射v_NGF后兔眼玻璃体内药物浓度在 6h达高峰 ;而玻璃体内注射在 1h达高峰并能在眼内达到较高的药物浓度及维持较长时间。结论　玻璃体内注射v_NGF后 ,该药在眼内有良好的分布。     

玻璃体腔注射曲安奈德治疗52例黄斑水肿疗效分析

[背景]观察玻璃体腔内注射曲安奈德治疗黄斑水肿的疗效.[病例报告]52例患者均经荧光素眼底血管造影检查确诊为黄斑水肿,其中糖尿病性重度弥漫性黄斑水肿者为29例,视网膜中央静脉阻塞所致的囊样黄斑水肿者为15例,颞侧分支静脉阻塞所致的黄斑水肿者为8例,均给予玻璃体腔内注射曲安奈德4 mg(0.1 mL).随访1~10个月,观察患者视力、眼压、眼底情况及炎症反应,并应用荧光素眼底血管造影观察视网膜渗漏情况.52例中46例视力提高,效果最佳者视力由治疗前0.1提高至0.6,6例的视力无变化;眼压升高者为2例,其中1例眼压高达6.80 kPa;水肿复发者为4例.[讨论]玻璃体腔内注射曲安奈德治疗黄斑水肿有一定的疗效,但部分患者治疗后出现复发,并可见发生眼压升高等不良反应.     

Management of Infectious Endophthalmitis

Diagnostic anterior chamber and vitreous aspiration confirmed an infectious etiology in 78 of 140 eyes (56%) with suspected endophthalmitis. In 27 eyes the vitreous aspirate was positive, while the anterior chamber aspirate was negative. Intraocular antibiotics were used in 88 eyes including 50 which underwent therapeutic vitrectomy. Vision of 20/20 to 20/400 was achieved in 57% of recently operated, culture-positive eyes treated with intraocular antibiotics, and in 59% of those treated with combined vitrectomy and intraocular antibiotics.     

Vascular accidents in preretinal arterial loops

Three cases with preretinal arterial loops complicated by obstructive accidents of various intensities are reported. The range of the complication varied from arterial spasm to transient retinal hemorrhages and arterial branch occlusion with permanent field defect, followed by extensive recurrent vitreous hemorrhages. These results lend further support to the assumption that the spiral arterial loops have an inherent tendency to twist and produce occlusive episodes.     

Preoperative Prognostic Factors in Diabetic Pars Plana Vitrectomy

The postoperative, six-month visual acuities of 1056 diabetic vitrectomy cases were compared to the following preoperative findings: duration of decreased vision associated with detachments, pupillary responses, iris rubeosis, intraocular tensions, extent of neovascularization, macular status, the ability to recognize entoptic phenomena, bright-flash ERG, and ultrasonography. By comparing these findings to the postoperative visual results, several factors were detected that could be helpful in determining the preoperative prognosis for improved vision. However, major operative complications reduced the incidence of successful visual results from 53% to 22%.     

Lens injury stimulates adult mouse retinal ganglion cell axon regeneration via both macrophage- and lens-derived factors

In the present study the effects of lens injury on retinal ganglion cell axon/neurite re-growth were investigated in adult mice. In vivo, lens injury promoted successful regeneration of retinal ganglion cell axons past the optic nerve lesion site, concomitant with the invasion of macrophages into the eye and the presence of activated retinal astrocytes/Muller cells. In vitro, retinal ganglion cells from lens-lesioned mice grew significantly longer neurites than those from intact mice, which correlated with the presence of enhanced numbers of activated retinal astrocytes/Muller cells. Co-culture of retinal ganglion cells from intact mice with macrophage-rich lesioned lens/vitreous body led to increased neurite lengths compared with co-culture with macrophage-free intact lens/vitreous body, pointing to a neurotrophic effect of macrophages. Furthermore, retinal ganglion cells from mice that had no lens injury but had received intravitreal Zymosan injections to stimulate macrophage invasion into the eye grew significantly longer neurites compared with controls, as did retinal ganglion cells from intact mice co-cultured with macrophage-rich vitreous body from Zymosan-treated mice. The intact lens, but not the intact vitreous body, exerted a neurotrophic effect on retinal ganglion cell neurite outgrowth, suggesting that lens-derived neurotrophic factor(s) conspire with those derived from macrophages in lens injury-stimulated axon regeneration. Together, these results show that lens injury promotes retinal ganglion cell axon regeneration/neurite outgrowth in adult mice, an observation with important implications for axon regeneration studies in transgenic mouse models.     

Dexamethasone regulates endothelin-1 and endothelin receptors in human non-pigmented ciliary epithelial (HNPE) cells

Endothelin-1 (ET-1) lowers intraocular pressure (IOP) in animal models by regulating aqueous humour dynamics through both inflow and outflow mechanisms. Moreover, ET's concentration is elevated in glaucoma patients and in animal models of glaucoma. Glucocorticoid therapy often can lead to increase IOP in susceptible individuals including patients with primary open angle glaucoma (POAG). In this study, we examined the effects of dexamethasone (Dex), a frequently used anti-inflammatory glucocorticoid, on the synthesis and release of endothelin-1 and on the expression of endothelin receptors in human non-pigmented ciliary epithelial (HNPE) cells, an established source for ET-1 in the anterior chamber. As measured by ET-1 immunoreactivity, ET-1 was concentration-dependently increased following 24hr Dex treatment, with a maximum concentration (100 nM) causing a threefold increase of ET-1 release. Western blot analysis of HNPE cells showed the expression of endothelin receptor A (ET(A)) and endothelin receptor B (ET(B)) with approximate molecular weights of 40 kDa. Dex treatment decreased ET(A) receptor expression at all Dex doses, but up-regulated ET(B) receptors with 10nM Dex having the greatest effect. Quantitative PCR demonstrated that Dex also increased the mRNA of pre-pro-ET-1 (ppET-1) and ET(B) but decreased the mRNA of ET(A). RU486, a glucocorticoid receptor antagonist, was able to block Dex's actions on ET release and ET(B) receptor expression, but did not block its action on ET(A) receptor expression. Endothelin receptors were minimally expressed in HNPE cells as determined in binding experiments (B(max): ET(A) 17, ET(B) 25 fmolmg(-1) membrane protein). However Dex treatment stimulated a dramatic increase in ET(B) receptor density while decreasing ET(A) receptors (B(max): ET(A) 11, ET(B) 116 fmolmg(-1) membrane protein). The regulation of endothelin and its receptors could be a novel mechanism associated with glucocorticoid's effects on intraocular pressure. The increase in ET-1 and disproportionate regulation in ET receptor expression by Dex could promote dysregulation in ET's mechanism on both inflow and outflow, thus affecting aqueous humour dynamics in the anterior chamber of the eye.     

糖尿病患者玻璃体积血病因分析

目的:分析糖尿病患者玻璃体出血的原因,为相关疾病的诊治提供资料。方法:对2004-04/2007-06我科收治的126例(142眼)玻璃体积血的糖尿病患者情况进行回顾性分析。结果:增殖性糖尿病视网膜病变(proliferative diabetic reti-nopathy,PDR)122眼(85.9%),视网膜静脉阻塞(retinal vein occlusion,RVO)10眼(7.0%),视网膜裂孔(retinal hole,RH)6眼(4.2%),玻璃体后脱离(posterior vitreous detachment,PVD)4眼(2.8%);PDR组患者对侧眼糖尿病视网膜病变显著重于其余各组。结论:增殖性糖尿病视网膜病变是糖尿病患者玻璃体出血的主要原因,此外,视网膜静脉阻塞、视网膜裂孔和玻璃体后脱离也占有一定比例;通过对侧眼情况的评估,有助于玻璃体出血原因的判断。