基质金属蛋白酶在孔源性视网膜脱离视网膜下液的定量研究

目的 研究孔源性视网膜脱离(RRD)视网膜下液(SRF)基质金属蛋白酶(MMPs)的表达，探讨MMPs与增生性玻璃体视网膜病变(PVR)的关系。方法 采用明胶酶谱分析法定量检测88例RRD患者的SRFMMP-2和MMP-9的活性水平，PVR A组21例，PVRB组37例，PVR C组30例，其中包括伴有脉络膜脱离RRD8例，术后随访PVR复发11例。结果 88例RRD患者的SRF均有MMP-2活性水平升高，33例有MMP-9的表达，8例RRD伴有脉络膜脱离，有6例(75％)MMP-9活性水平升高，术后PVR复发11例SRF均有MMP-9活性水平升高。结论RRD患者的SRF有MMP-2和MMP-9的表达，MMP-9活性水平升高可能与PVR的发生有关，可能成为预测术后PVR复发的指标之一。     

基质金属蛋白酶在视网膜前膜的表达和意义

目的 研究增生性玻璃体视网膜病变（PVR）视网膜前膜中基质金属蛋白酶（MMPs)的表达。探讨MMPs在PVR病理过程中的作用。方法 经扁平部玻璃体切割术（PPV）和膜剥离术取得PVRC3-D3级视网膜前膜21例，免疫组织化学法分析MMP-2和MMP-9在PVR视网膜前膜的表达，同时进行视网膜色素上皮细胞（RPE）和巨噬细胞染色。结果 21例PVR视网膜前膜MMP-2阳性染色15例，MMP-9阳性8例，RPE细胞表达18例，巨噬细胞表达9例。结论 PVR视网膜前膜有MMP-2和MMP-9表达，可能主要由RPE细胞和巨噬细胞分泌，对PVR的发生和发展起重要作用。     

内层视网膜从玻璃体腔摄取氧的初步研究

目的　研究内层视网膜从玻璃体腔摄取氧的可能性。方法　对兔眼行玻璃体切割术 ,使玻璃体腔被较富氧的灌注液填充 ,利用光纤测氧仪监测玻璃体腔内氧分压的改变。结果　对 6只兔进行实验 ,玻璃体中央的氧分压为( 15 9± 2 8)mmHg( 12眼 ) ;在 6只玻璃体切割眼中 ,玻璃体切割结束时玻璃体腔内灌注液的氧分压为 ( 119 3± 18 9)mmHg ,经过 ( 2 6 3± 11 8)min ,氧分压降低到 ( 2 8 9± 12 2 )mmHg并维持稳定。 结论　内层视网膜具有相当高的从玻璃体腔摄取氧的能力。     

玻璃体切除联合曲安奈德玻璃体腔注射治疗孔源性视网膜脱离

目的 探讨玻璃体切除联合曲安奈德(TA)玻璃体腔内注射治疗合并脉络膜脱离的孔源性视网膜脱离的临床疗效和安全性.方法 观察采用玻璃体切除联合曲安奈德玻璃体腔内注射治疗合并脉络膜脱离的孔源性视网膜脱离15例患者(15眼),术后不再全身应用糖皮质激素,仅给予激素眼液点眼.结果 术后随访时间6～30个月,平均(19±9.5)个月.一次手术视网膜复位率100%.术后3个月硅油取出后,2例视网膜脱离复发,1例再次剥膜充填硅油后视网膜复位;另1例放弃治疗.视网膜总复位率为93.3%(14/15).术后并发症包括:4例术后眼压升高,均局部用药控制,5例出现晶状体后囊下皮质局限性混浊.结论 玻璃体切除联合(TA)玻璃体腔内注射治疗合并脉络膜脱离的孔源性视网膜脱离,可以明显减轻术后葡萄膜炎症反应,从而减少PVR的发生,显著提高手术的成功率.     

玻璃体切除联合眼内填充治疗复杂视网膜脱离

目的　探讨复杂性视网膜脱离应用玻璃体切除联合眼内填充手术的效果及并发症的发生情况。方法　对2 9例伴有眼球破裂伤、眼内炎、玻璃体积血、白内障、PVR或糖尿病性视网膜病变等的复杂性视网膜脱离进行玻璃体视网膜手术的连续病例临床资料进行回顾性分析。结果　玻璃体切除联合玻璃体腔注气术12眼,1次手术视网膜复位8眼(66.67%) ;玻璃体切除联合玻璃体腔内硅油填充术2 0眼(包括注气失败的3眼) ,1次手术完全复位13眼(65 .0 0 %)。统计学检验两组1次手术视网膜复位率的差异无显著意义。术后视力较术前提高者2 1眼(72 .41%)。常见的并发症有复发性视网膜脱离、并发性白内障及继发性青光眼等。结论　玻璃体切除联合眼内填充能有效地治疗复杂性视网膜脱离,PVR仍然是术后视网膜脱离复发的主要因素。     

玻璃体切除治疗无严重增殖性玻璃体视网膜病变的视网膜脱离

目的:探讨后段玻璃体切除术(PPV)在非严重性增殖性玻璃体视网膜病变(PVR)性视网膜脱离中的作用。方法:研究15眼有裂孔边缘卷曲的PVR—B级网脱,11眼裂孔在赤道后的PVR—C1或C2级网脱及28眼眼底可视度差的网脱共54眼,用玻璃体切除治疗的效果。结果:一次手术成功率为76％,总成功率96％。术后视力提高43眼(79.6％),不变9眼(16.7％),变坏2眼(3.7％)。结论:PPV是治疗一些非复杂性网脱的有效及安全的方法。眼科学报1998;14:97—99。     

自制玻璃体气液交换装置在增生期糖尿病视网膜病变患者玻璃体切术后玻璃体腔积血的临床应用

目的 观察自制玻璃体腔气液交换装置在增生期糖尿病视网膜病变(PDR)患者接受玻璃体切除术(PPV)后，再次出现玻璃体腔积血的临床效果。方法 随机对照研究。选取2019年10月至2021年1月期间在上海市松江区中心医院眼科住院并接受PPV的PDR患者43例(52只眼),随机分成观察组(玻璃体腔气液交换装置进行气液交换术)23例(27只眼)和对照组(玻璃体腔灌洗术)20例(25只眼)。比较两组不同时期平均最佳矫正视力(BCVA)变化情况，术后复发性玻璃体积血(VH)、外伤性白内障、糖尿病性黄斑水肿(DME)、抗VEGF治疗等情况。结果 两组患者术前一般情况差异无统计学意义(均P>0.05);观察组平均手术持续时间明显低于对照组(P<0.05);1周内观察组术后平均BCVA低于对照组(均P<0.05);术后1周及后续的随访中，观察组和对照组平均BCVA差异无统计学意义(均P>0.05);复发性VH、DME的发生率差异均无统计学意义(均P>0.05)。结论 自制玻璃体腔气液交换装置可以很好地将PDR患者PPV术后玻璃体腔血水交换出来，提高视力，无明显并发症发生。     

基质金属蛋白酶在翼状胬肉的表达

目的:研究基质金属蛋白酶(matrix metalloproteinases,MMPs)在翼状胬肉中的分布和活性状态,探讨MMPs在翼状胬肉病理过程中的作用。方法:翼状胬肉切除术患者26例27只眼,静止期18只眼,进行期9只眼,正常人球结膜6例,免疫组织化学法和明胶酶谱法分析MMP-2和MMP-9的表达和活性水平。结果:翼状胬肉标本有MMP-2和MMP-9表达,MMB-2主要分布在基底上皮细胞层,MMP-9在炎症细胞和血管内皮细胞有阳性染色,翼状胬肉静止期MMP-2的活性水平[(235±18.17)扫描单位]和进展期[(221±22.53)扫描单位]比较差异无显著意义(P>0.05),MMP-9活性水平在静止期[(46±32.21)扫描单位]和进展期[(159±19.28)扫描单位]比较差异有显著性意义(P<0.05)。结论:翼状胬肉中MMP-2和MMP-9表达增强,MMP-2和MMP-9活性水平升高可能与翼状胬肉的发展有关。     

网脱术中阿霉素和地塞米松眼内注射的观察

目的应用阿霉素及地塞米松在网脱术中注入玻璃体腔,观察对增生性视网膜玻璃体病变(PVR)的抑制作用.方法对42例视网膜脱离伴PVR的患者施行手术加玻璃体腔药物注射,与单纯手术组30眼视网膜脱离伴PVR作对比分析,并行有关血流动力学观察.结果手术加注药物组与单纯手术组比较,术后3～5月视网膜表面增生膜和网膜下机化膜比术前加重的发生率分别为7.14%和26.67%,x2检验P＜0.05.两组环扎术均可导致眼部血流动力学改变,术后1～2周的视网膜中央动脉和中央静脉的收缩期最大平均流速分别为(6.31±2.5)cm/s和(4.77±1.4)cm/s,比正常值分别下降33.66%和16.66%.结论此方法是防治PVR的一种有价值的方法.     

地塞米松缓释微粒在增生性玻璃体视网膜病变的应用

目的：观察含地塞米松（DEX）的缓释微粒治疗增生性玻璃体视网膜病变（PVR）的临床疗效。方法：9例（9只眼）视网膜脱离伴PVR患者进行常规玻璃体视网膜手术，并在玻璃体腔内植入1粒DEX微粒（含地塞米松1mg），观察术后反应及视力、PVR发展、DEX的位置及形状变化等。结果：术后炎症反应轻，7只眼视网膜复位，3只眼后极部视网膜前有增生；2只眼视网膜局限性脱离，最终3只眼玻璃腔内硅油填充。随访视力有8只眼较术前提高（P=0.015）。DEX未见对视网膜有不良影响，仅在随着处有少量色素吸附，4-6月后吸收。结论：DEX抑制PVR术后炎症反应及较远期作用是安全、有效的；对手术未完全清除的视网膜前增生有一定的抑制作用。     

The activated form of gelatinase B/matrix metalloproteinase-9 is associated with diabetic vitreous hemorrhage

We aimed to investigate the presence and activation status of matrix metalloproteinase (MMP)-2 and MMP-9 in vitreous samples from proliferative diabetic retinopathy (PDR) patients. Paired vitreous and serum samples were obtained from patients undergoing vitrectomy for the treatment of rhegmatogenous retinal detachment (RD) (65 patients) and PDR (67 patients). PDR patients were diagnosed for the presence of hemorrhage and/or patent new vessels. Quantitative assays were performed for vitreous protein content, MMP-2, MMP-9, tissue inhibitor of metalloproteinases-1 (TIMP-1) and hemoglobin. Qualitative evaluation of the MMP-2 and MMP-9 activation status was performed by zymography. Vitreous samples contained proMMP-2 but levels were unselectively related to total protein content. ProMMP-9 and activated MMP-9 levels were significantly increased in PDR patients (p<0.001 for both comparisons). In addition, TIMP-1 levels were significantly increased in PDR patients (p=0.004) and functionally inhibited activation of MMP-9 in vitreous samples. None of the parameters significantly differed between PDR patients with patent new vessels and those with inactive disease. However, activated MMP-9 levels in vitreous samples of PDR patients with hemorrhage (75.7+/-106.3 scanning units per 2 microl) were significantly higher than those in PDR patients without hemorrhage (7.1+/-16.2 scanning units per 2 microl) (p<0.001) and strongly correlated with hemoglobin levels (r=0.7525; p<0.001). Activated MMP-9 was not detected in paired serum samples. We conclude that activated MMP-9 might be involved in hemorrhagic transformation in patients with PDR.     

Correlation of matrix metalloproteinase levels with the grade of proliferative vitreoretinopathy in the subretinal fluid and vitreous during rhegmatogenous retinal detachment

Purpose: We investigated the activity of matrix metalloproteinase (MMP)‐2 and ‐9 and their latent pro‐forms (proMMP‐2, ‐9), and protein levels of MMP‐1, ‐3, ‐8 and tissue inhibitor of MMPs (TIMP)‐1 in the subretinal fluid (SRF) and vitreous of patients with rhegmatogenous retinal detachment (RRD). Potential correlations with proliferative vitreoretinopathy (PVR) grade were determined. Methods: Thirty‐seven SRF and 32 vitreous samples from RRD patients and nine vitreous samples from human organ donors (controls), were collected and assayed for MMP‐1, ‐3, ‐8/TIMP‐1 levels using enzyme‐linked immunosorbent assay (ELISA), and for proMMP‐2, ‐9, MMP‐2, ‐9 activity employing gelatine zymography. Results: ProMMP‐2, ‐9, MMP‐1, ‐3, ‐9, TIMP‐1 were significantly higher in the SRF and vitreous of RRD patients compared to the vitreous of organ donors. MMP‐8 levels were higher in RRD patients’ SRF. Regarding PVR grade, MMPs and TIMP‐1 were differentially present in SRF and vitreous. PVR grade correlated significantly with the levels of MMP‐2 in SRF, while proMMP‐2, MMP‐1, ‐2, ‐3, ‐8, ‐9 and TIMP‐1 levels correlated with PVR grade in the vitreous. Conclusion: MMP/TIMP‐1 levels are elevated in SRF and vitreous during RRD. Significant correlations between PVR grade and MMP‐2 in SRF and proMMP‐2, MMP‐1, ‐2, ‐3, ‐8, ‐9 and TIMP‐1 levels in vitreous were revealed. Investigation of MMP activity in vitreous may provide more valid conclusions compared to SRF pertaining to the role of the MMPs during RRD. The observations of the present study suggest a possible role for MMPs and TIMP‐1 in PVR pathophysiology.     

增生性玻璃体视网膜病变玻璃体中的Ⅲ型前胶原

目的:检测增生性玻璃体视网膜病变(PVR)患者血清及玻璃体中Ⅲ型前胶原(Procollagen Ⅲ,PC Ⅲ)的含量,探讨其在PVR发病中的作用。方法:用放射免疫测定法测定5例正常人玻璃体,20例正常人血清及29例孔源性视网膜脱离合并PVR患者玻璃体及血清中的PC Ⅲ。用Logistic回归模型分析PVR患者发病时间、手术史、增生膜及PVR分级与PC Ⅲ含量的相关性。结果:PVR患者血清和对照组血清PC Ⅲ含量分别为83.76±18.52和85.02±17.50μg/L(P>0.05)。正常对照玻璃体PC Ⅲ含量低于最小可测值(40 μg/L)。PVR患者组中有12例未检测到,其余17例玻璃体中PC Ⅲ含量明显升高,平均268.69±176.07μg/L(P<0.05)。玻璃体PC Ⅲ水平与病史长短和PVR级别相关,发病时间延长,其玻璃体PC Ⅲ含量大于40μg/L的概率是小于40 μg/L的5.2655倍;PVR级别增加,其玻璃体PC Ⅲ含量大于40 μg/L的概率是小于40 μg/L的2.7978倍。结论:多数PVR患者玻璃体内可测得PC Ⅲ含量增加,并与PVR分级及发病时间长短相关。PC Ⅲ合成活跃属眼内的局部反应。提示PC Ⅲ及Ⅲ型胶原在PVR发展中起一定的作用。眼科学报1998;14:76—79。     

Correlation of the extent and duration of rhegmatogenous retinal detachment with the expression of matrix metalloproteinases in the vitreous

BACKGROUND: Investigation of the activity of matrix metalloproteinase (MMP)-2 and -9 and protein levels of MMP-1, -3, -8, and the tissue inhibitor of MMPs (TIMP)-1 in the vitreous of patients with rhegmatogenous retinal detachment (RRD) and establishment of potential correlations of MMPs with clinical parameters. METHODS: Thirty-two vitreous samples from patients with RRD and 9 vitreous samples from human organ donors (controls) were assayed for MMP-1,-3, -8, and TIMP-1 levels using enzyme-linked immunosorbent assay and MMP-2 and -9 activity employing gelatin zymography. RESULTS: MMP-1, MMP-3, proMMP-2, proMMP-9, MMP-9, and TIMP-1 were higher in vitreous from patients with RRD as compared to organ donors. Overall, MMPs and TIMPs were differentially expressed in vitreous from RRD with respect to the duration and extent of RRD. Regression analysis for all data indicated that a model consisting of MMP-2 and TIMP-1 could estimate the extent of RRD. CONCLUSION: Levels of MMPs and TIMP-1 studied are elevated in vitreous during RRD. MMP-2 and TIMP-1 may have a more prominent and persistent role than other MMPs in the wound healing process of the retina during RRD. A regression model consisting of MMP-2 and TIMP-1 may prove to be of potential use in providing information for the evaluation of the extent of RRD.     

三种视网膜病视网膜前膜中基质金属蛋白酶及其天然抑制分子的表达

目的 研究增殖性糖尿病视网膜病变(proliferative diabetic retinopathy,PDR)、增殖性玻璃体视网膜疾病(proliferative vitreoretinopathy,PVR)和急性视网膜坏死(acute retinalnecrosis,ARN)患者视网膜前膜中基质金属蛋白酶(matrixmetalloproteinases:MMPs)及其天然抑制物(tissueinhibitorsofmetalloproteinages,TIMPs)的表达情况.方法 玻璃体手术中剥取PVR、PDR和ARN患者的视网膜前膜,同供体眼视网膜作为正常对照,冰冻切片后进行免疫组织化学染色,包括:MMP-1,MMP-2,MMP-3,MMP-7,MMP-9,TIMP-1和TIMP-2.结果 正常视网膜中能够观察到MMP-1,MMP-3,TIMP-1和TIMP-2的表达,在PVR、PDR和ARN患者标本中各种分子的表达都增强,尤以MMP-2,MMP-3和MMP-7明显.结论 正常视网膜中存在MMPs和TIMPs分子维持着细胞外基质动态的平衡,在PVR,PDR和ARN患者中MMP-2,MMP-3和MMP-7等MMPs分子表达增强,在其病变过程中可能起重要作用.     

Matrix metalloproteinases in epithelia from human recurrent corneal erosion

PURPOSE: To assay for the presence of matrix metalloproteinases (MMPs) in human corneal epithelium affected by recurrent erosion compared with that in normal corneal epithelium. METHODS: Corneal epithelial debridement samples were obtained from 13 patients with recurrent epithelial erosion. For control specimens, epithelia were obtained from healthy patients undergoing photorefractive keratectomy. Zymography was performed on all samples to identify MMPs. Immunolocalization of MMP-2, laminin, and collagen type VII was determined in two samples with human recurrent epithelial erosion and compared with that in control epithelium. RESULTS: Twelve of 13 erosion samples showed MMP-2 enzymatic activity; one of the 12 also showed MMP-9 activity. Only one erosion sample showed no MMP enzymatic activity. All normal control specimens were negative for MMP. Immunohistochemical analysis of two recurrent erosion samples showed MMP-2 presence in basal cells, whereas, in normal epithelium it was not detected. One sample with epithelial erosion showed laminin localization in basal epithelial cells and basal lamina. Type VII collagen localized in basal epithelial cells only in this sample. A second erosion sample showed localization of laminin and type VII collagen in basal epithelial cells only. Normal corneal epithelium showed presence of laminin and type VII collagen in basal epithelium and basal lamina. CONCLUSIONS: Matrix metalloproteinase-2 expression is upregulated in human epithelia affected by recurrent erosion compared with that in normal control samples. Immunolocalization studies suggest that this enzyme is concentrated in basal epithelial cells where it may play an important role in degradation of the epithelial anchoring system and the recurrent epithelial slippage and erosion observed in these patients.     

Decrease of the postoperative inflammatory reaction during pars plana vitrectomy (PPV) after administration of triamcinolone acetonide

PURPOSE: To prospectively evaluate the effect on postoperative inflammatory reaction and recovery after application of triamcinolone acetonide (TA) during pars plana vitrectomy (PPV), to visualize the vitreous. MATERIAL AND METHODS: Pars plana vitrectomy (PPV) was performed in 45 patients (21 males, 24 females) (29 with retinal detachment, 6 with macular hole, 1 with cystoid macular edema, 3 with diabetic retinopathy, 3 with vitreous haemorrhage, 1 with preretinal membrane, 1 with PVR and 1 with lens luxation). After surgical separation of the posterior vitreous and removal of any visible epiretinal membrane, TA was injected over the posterior pole. For the control group we used 15 patients (10 with retinal detachment, 2 with macular hole, 1 with preretinal membrane, 1 with lens luxation and 1 with vitreous haemorrhage) (10 males, 5 females) treated with PPV but without TA administration. To evaluate the degree of postoperative inflammation and to monitor the dynamics of the blood-aqueous barrier disruption, the laser flare cell meter (Kowa FM-500) was used. RESULTS: Tyndalometric mean values in the control group of eyes recorded 1 day after PPV were 32.41 +/- 6.1 ph/ msec while values in TA-treated group were significantly lower (20.26 +/- 2.4, p < 0.02). 10 days after surgery in TA group results were still significantly lower as compared to the control group (16.4 +/- 2.6 vs 32.5 +/- 9.6, p < 0.005). As observed 6 weeks after PPV, tyndalometric recordings in TA-treated group remained lower as those observed in the control group (16.1 +/- 3.1 vs 32.0 +/- 8.1, p < 0.01). CONCLUSIONS: The eyes which received TA-assisted PPV showed significantly less breakdown of the blood-ocular barrier than those with routine PPV. Intraoperative administration TA facilitates postoperative recovery after surgery lowering the inflammatory reaction.     

Interleukin-8, nitric oxide and glutathione status in proliferative vitreoretinopathy and proliferative diabetic retinopathy

PURPOSE: To evaluate interleukin-8 (IL-8), nitric oxide (NO) and glutathione (GSH) profiles in vitreous humor and blood samples in patients with proliferative diabetic retinopathy (PDR) and in patients with proliferative vitreoretinopathy (PVR) and to compare the levels with those of controls. PATIENTS AND METHODS: NO concentrations were determined by using the Greiss reaction in plasma and vitreous humor samples. GSH levels were determined in both blood and vitreous humor samples, using DTNB, a disulfide chromogen. Vitreous IL-8 were assayed by ELISA. Twenty-three patients with PDR, 18 patients with PVR and 21 cadavers as the control group were included in the study. RESULTS: Plasma and vitreous NO levels were found to be 25.6 +/- 2.1 and 36.9 +/- 3.0 micromol/l in patients with PDR, 27.0 +/- 4.7 and 34.3 +/- 2.9 micromol/l in patients with PVR and 17.4 +/- 2.7 and 15.9 +/- 1.4 micromol/l in controls, respectively. Vitreous humor and plasma NO levels did not show any statistically significant difference between PDR and PVR groups. However, the values for vitreous in both groups were significantly higher than those of controls (p < 0.0001). Although IL-8 levels in vitreous samples of patients with PDR were not significantly different (79.6 +/- 9.7 pg/ml) from those of patients with PVR (42.2 +/- 7.3 pg/ml) (p = 0.06), the levels in both groups were significantly higher than those of controls (19.0 +/- 3.9 pg/ml) (p < 0.0001 and p < 0.05, respectively). Blood and vitreous GSH levels were found to be 5.3 +/- 0.4 micromol/g. Hb and 0.58 +/- 0.16 micromol/l in patients with PDR and 8.4 +/- 0.5 micromol/g. Hb and 15.7 +/- 2.2 micromol/l in patients with PVR and 12.0 +/- 1.1 micromol/g. Hb and 0.26 +/- 0.03 mmol/l in controls, respectively. Vitreous and blood GSH levels were significantly lower in patients with PDR compared to those with PVR (p < 0.0001 for both). CONCLUSION: Elevated levels of vitreous and plasma NO and vitreous IL-8 in PDR and PVR implicate a role for these parameters in the proliferation in these ocular disorders. GSH concentrations both in vitreous and blood samples of the PVR and PDR patients were much less than those observed in the control group. Lower GSH concentrations detected in PDR in comparison with those in PVR in vitreous humor and to a lesser degree in blood may play an important role in pathogenesis of new retinal vessel formation in patients with PDR. This also suggests that oxidative stress may be involved in the pathogenesis of PVR and particularly that of PDR.