t—PA结膜下注射治疗术后眼内纤维蛋白渗出

为观察ｔ－ＰＡ（组织型纤溶酶原激活剂）结膜下注射对术后眼内纤维蛋白渗出的治疗效果，对２０例（２０眼）术后眼内纤维蛋白渗出患者用ｔ－ＰＡ结膜下注射。ｔ－ＰＡ治疗浓度为５０μｇ／ｍｌ，每次注射剂量为０．５ｍｌ，一次注射不能使纤维蛋白渗出完全溶解者间隔４８～７２小时重复给药，直至吸收。并与同期１９例（１９眼）用地塞米松治疗眼内纤维蛋白渗出的病人作对照。结果表明ｔ－ＰＡ组眼内纤维蛋白渗出完全吸收时间为注药后１～１４天，平均５．２０±３．４９天。对照组纤维蛋白渗出完全吸收时间为１～２１天，平均１０．３２±５．９６天，二者相比，有显著差异（Ｐ＜０．０１）。在ｔ－ＰＡ组治疗中未发现出血倾向、眼内压升高等并发症。全组病人随访一个月，未见眼内纤维蛋白渗出复发。认为ｔ－ＰＡ结膜下注射治疗眼内纤维蛋白渗出为一种安全有效的治疗方法。     

组织型纤溶酶原激活剂对实验性前房出血的治疗观察

组织型纤溶酶原激活剂对实验性前房出血的治疗观察赵培泉，王文吉，宋后燕，朱运松基因工程生产的组织型纤溶酶原激活剂（ｔ－ＰＡ）已被证实是一高效、特异的新型纤维蛋白溶解剂。我们通过实验拟观察ｔ－ＰＡ对实验性前房出血的治疗作用。１．材料与方法：取健康成年日本...     

t—PA在青光眼滤过性手术中的应用

组织型纤溶酶原激活剂（ｔ－ＰＡ）是一种新型溶栓酶，可用来水解青光眼滤过性手术后滤过口内的纤维蛋白凝块，减少手术区的瘢痕化，提高手术成功率。本对ｔ－ＰＡ的理化特性、动物实验、临床应用以及毒副作用等方面进行了综述，展示了ｔ－ＰＡ在青光眼手术中的良好应用前景。     

t-PA结膜下注射治疗术后眼内纤维蛋白渗出

目的：观察ｔ－ＰＡ（组织型纤溶酶原激活剂）结膜下注射对术后眼内纤维蛋白渗出的治疗效果。方法：对２０例（２０只眼）术后眼内纤维蛋白渗出患者用浓度为５０μｇ／ｍｌｔ－ＰＡ结膜下注射。每次注射０．５ｍｌ，一次注射不能使纤维蛋白渗出完全溶解者间隔４４８￣７２小时重复给药，直至吸收。并与同期１９例（１９只眼）用激素治疗眼内纤维蛋白渗出的患者作对照。结果：ｔ－ＰＡ组眼内纤维蛋白完全溶解时间为注药后１￣１４天，     

t—PA和5—Fu多相脂质体联合应用对兔青光眼滤过术后瘢痕形成的影响

研究组织纤溶酶原激活剂（ｔｉｓｓｕｅ ｐｌａｓｍｉｎｏｇｅｎ ａｃｔｉｖａｔｏｒ，ｔ－ＰＡ）联合５－氟尿嘧啶（５－Ｆｌｕｏｒｏｕｒａｃｉｌ，５－Ｆｕ）多相脂质体抑制青光眼滤后瘢痕形成的作用。方法将１６只健康成年新西兰长耳兔随机分成４组，每组１只，均行双眼小梁切除术。第１组：为对照组，手术结束时双眼前房内各注射生理盐水０．１ｍｌ，共４次。术后不用抑制瘢痕形成的药物。第２组；手术结束时双眼前房内注射ｔ     

t－PA对实验性玻璃体渗出的治疗作用

１８只兔眼玻璃体腔内注射自体血浆０．２ｍｌ制成的玻璃体渗出模型，随机接受玻璃体内注射组织型纤溶酶原激活酶（ｔ－ｐＡ）或生理盐水，其中１０眼玻璃体内注入ｔ－ＰＡｌ２．５μｇ，结果６眼的纤维蛋白在６ｈ内清除，另４眼在ｌｄ内彻底清除。注入生理盐水的７眼需７ｄ才完全清除。两组从时间上比较，差别有显著性（Ｐ＜０．０５）．经裂隙灯、ＥＲＧ、光镜及电镜检查未见毒性作用。另１只注入１００μｇｔ－ＰＡ的兔眼虽然６ｈ内见纤维蛋白凝块溶解，但眼底镜和光镜下已显示视网膜的毒性变化。     

组织型纤溶酶原激活剂（t—PA）给药途径的探讨

组织型纤溶酶原激活剂（ｔ—ＰＡ）给药途径的探讨上海医科大学眼科医院赵培泉，王文吉上海医科大学分子遗传室宋后燕，朱运松目前临床上ｔ－ＰＡ的给药途径是直接注入眼内。这种方法操作麻烦，也增加感染与损伤组织的机会，如能选用别的给药方法并能取得同样的效果，则可...     

血栓通联合等容血液稀释治疗视网膜静脉阻塞对纤溶活性及血液流变学的影响

目的探讨血栓通（ｐａｎａｘｎｏｔｏｇｉｎｓａｎｇｓａｐｏｎｉｎｓ，ＰＮＳ）、等容血液稀释（ｉｓｏｖａｌａｅｍｉｃｈａｅｍｏｄｉｌｕｔｉｏｎ，ＩＨＤ）以及二者联合治疗视网膜静脉阻塞（ｒｅｔｉｎａｌｖｅｉｎｏｃｃｌｕｓｉｏｎ，ＲＶＯ）的效果。方法采用ＰＮＳ、ＩＨＤ及二者联合随机对照治疗ＲＶＯ患者７３例，观察治疗前后患者血浆组织型纤溶酶原激活物（ｔｉｓｓｕｅｐｌａｓｍｉｎｏｇｅｎａｃｔｉｖａｔｏｒ，ｔ－ＰＡ）及其抑制物（ｐｌａｓｍｉｎｏｇｅｎａｃｔｉｖａｔｏｒｉｎｈｉｂｉｔｏｒ，ＰＡＩ）活性、血液流变学参数及视力的改变。结果治疗结束时，ＰＮＳ＋ＩＨＤ组和ＰＮＳ组较治前ｔ－ＰＡ活性增高；ＰＡＩ活性降低；ＩＨＤ组ｔ－ＰＡ活性和ＰＡＩ活性改变不明显；除ＩＨＤ组血浆粘度变化不明显外，三组患者血液流变学指标均有不同程度改善。治疗后１个月，ＰＮＳ＋ＩＨＤ组全血低切粘度、低切还原粘度和红细胞聚集指数及其聚集力较治疗前仍有显著差异；且视力改善亦较快、较好。结论ＰＮＳ联合ＩＨＤ治疗ＲＶＯ具有调节机体纤溶功能和较持久地降低血液粘度，提高治疗效果的作用。     

糖尿病视网膜病变患者血浆tPA、PAI活性变化及意义

采用发色底物法检测了42例糖尿病视网膜病变(DR)患者和2l例正常人血浆组织型纤溶酶原激活剂(tPA)及纤溶酶原激活剂仰制物(PAl)活性，发现DR组tPA活性显著降低，PAI活性显著增高，且增殖型DR(PDR)组员显著(均P<0.01)。表明DR患者有血浆纤溶功能损害。提示血浆tPA、PAI活性变化以及两者之间的平衡失调在DR的发生发展中起着一定作用。 （中华眼底病杂志，1995，11：11-14）     

t—PA治疗玻璃体切割术后眼内纤维蛋白渗出

眼内纤维蛋白渗出是导致玻璃体切割术失败并危及视力的主要并发症之一。目前，动物实验和临床研究证实，玻璃体切割术联合眼部应用组织型纤维蛋白溶酶原激活剂（ｔ－ＰＡ），可有效地预防和治疗眼内纤维蛋白渗出及纤维增殖膜形成。本就这一疗法的研究现状作一总结，认为：眼部应用ｔ－ＰＡ治疗玻璃体切割术后眼内纤维蛋白渗出具有效果可靠、安全、毒性低、副作用小、适应证广泛等优点，在预防和治疗各种原因引起的增殖性玻璃体视网     

t-PA治疗玻璃体积血的实验研究

12只兔24眼玻璃体内注射自体血液0.2ml，制成玻璃体积血模型。均以右眼为对照眼，单纯注血；左眼为治疗眼，注血后不同时间玻璃体内注入组织型纤溶酶原激活剂(t-PA)12.5μg ，15天后活体摘除双眼球，光、电镜下观察组织学改变。结果表明：注血10天以后注药眼视网膜神经上皮、色素上皮病理改变较对照眼明显减轻。说明适时适量t-PA玻璃体内注射可减轻玻璃体积血对视网膜的损伤，为t-PA治疗玻璃体积血提供了组织学依据。 （中华眼底病杂志，1995，11：257-259）     

视网膜静脉阻塞患者血浆t-PA和PAI活性检测及临床意义

采用发色底物法检测61例视网膜静脉阻塞(RVO)患者血浆组织纤溶酶原激活剂(t-PA)及纤溶酶原激活剂抑制物(PAI)活性．正常对照组t-PA活性2.07±0.40IU/ml，PAI活性7.33±0.69AU/ml。RVO患者t-PA活性显著降低(1.69±0.56IU/ml，P<0.01)，PAI活性显著增高(8.80±1.60AU/ml，P<0.01)．其中缺血型较非缺血型t-PA活性吏低(分别为1.35±0.43IU/ml，1.92±0.53IU/ml，P<0，01)，PAI活性更高(分别为9.35±1.37IU/ml，8.42±1.29IU/ml，P<0.01)。并且，这些改变随病情严重程度的加重而愈显著． （中华眼底病杂志，1994，10：71-73）     

t-PA对实验性玻璃体渗出的治疗作用

18只兔眼玻璃体腔内注射自体血浆0.2ml制成的玻璃体渗出模型，随机接受玻璃体内注射组织型纤溶酶原激恬酶(t-PA)或生理盐水，其中10眼玻璃体内注入t-PA 12.5μg，结果6眼的纤维蛋白在6h内清除，另4眼在1d内彻底清除．注入生理盐水的7眼需7d才完全清除。两用从时间上比较，差别有显著性(P<0.05)．经裂隙灯、ERG、光镜及电镜检查未见毒性作用．另1只注入10μg t-PA的兔眼虽然6h内见纤维蛋白凝块溶解，但眼底镜和光镜下已显示视网膜的毒性变化。 （中华眼底病杂志，1994，10：14-16）     

t—PA眼内注射对实验性玻璃体出血的治疗观察

对小剂量组织型纤溶酶原激活制(t-PA)重复眼内注射治疗实验性玻璃体出血的疗效进行了观察.14只兔(28只眼)通过向玻璃体内注入0.05ml含枸橼酸钠的自体全血建立玻璃体出血模型。1周后将其随机分为3组，第1组和第2组隔周1次注射5μg或25μg-PA共注射2次(总量10μg或50μg)，第3组按同法接受生理盐水治疗．出血的清除在t-PA治疗组均显著地快于对照组(P<0.05或P<0.01)，但t-PA治疗组间差异无显著性．经ERG，光镜和电镜检查未见视网膜毒性变化。 （中华眼底病杂志，1995，11：185-187）     

Changes of Plasma tPA and PAI Activities in Patients with Diabetic Retinopathy

Purpose:To investigate the relationship between the diabetic retinopathy (DR) and the activity of plasma tissue plasminogen activator (tPA) and plasminogen activator inhibitor (PAI).Methods :tPA and PAI activities were measured by chromatogenous substrate assay in plasma samples obtained from patients with and without diabetic retinopathy (n = 42). Retinopathy was determined by stereoscopic color fundus photographs graded according to a modification of Chinese National Fundus Disease Academic Meeting. And 21 sex-age matched normal people were as controls. This study was in a masked fashion.Results:①tPA activity was lower and PAI activity was higher in all of diabetic patients than those in controls (P<0. 001); ②tPA activity was lower and PAI activity was higher in proliferative DR (PDR) subgroup than those in non-DR (NDR) and background-DR (BDR) subgroups (P<0.01,respectively); ③there was no significant difference between BDR and NDR subgroups (P>0. 05); and ④the results also suggested that the seve     

Fibrinolytic activity in retinal vein occlusion

Purpose: Impaired fibrinolytic function is a common finding in patients with thrombotic disease. The present study was initiated to evaluate the fibrinolytic response to a venous occlusion test (VOT) in patients with retinal vein occlusion. Methods: Euglobulin clot lysis time (ECLT), tissue plasminogen activator (t-PA) activity, and plasminogen activator inhibitor (PAI) activity were measured before and after VOT in a group of 26 consecutive patients presenting with retinal vein occlusion and in 15 healthy age- and sex-matched controls. Results: Before VOT (baseline), a higher proportion of patients (54%) had an ECLT of more than 5 h compared with controls (6.7%)(p = 0.0027) indicating decreased overall fibrinolytic activity. Patients had non-significantly lower t-PA and higher PAI activities compared with controls. After VOT, a higher proportion of patients (34.6%) had an ECLT of more than 5 h compared with controls (6.7%) (p = 0.05). Patients had significantly lower t-PA activity (p = 0.0232) and significantly higher PAI activity (p = 0.0292).Subgroup analysis revealed that patients with an ECLT of more than 5 h had significantly higher levels of PAI activity at baseline (p =0.0326) and after VOT (p = 0.0184) compared with patients with an ECLT of less than 5 hours. However, t-PA activity was significantly higher(p = 0.0153) at baseline, and non-significantly higher after VOT in patients with an ECLT of more than 5 h when compared with patients with an ECLT of less than 5 hours. Conclusions: These findings suggest that impaired fibrinolysis due to increased PAI activity may play a role in the pathogenesis of retinal vein occlusion. This revised version was published online in August 2006 with corrections to the Cover Date.     

Maspin increases extracellular plasminogen activator activity associated with corneal fibroblasts and myofibroblasts

Maspin, an inhibitor of cell migration and a stimulator of adhesion of cells to the ECM, is synthesized and released by corneal keratocytes into the extracellular matrix. When the cornea is wounded, the quiescent stromal keratocytes underlying the wound undergo apoptosis and cells adjacent to this apoptotic area convert to fibroblasts or myofibroblasts. This study explores the effect of extracellular maspin on the plasminogen–plasminogen activator system of corneal stromal cells following wounding. Treatment of corneal fibroblasts and myofibroblasts with r-maspin increased extracellular but not cell-associated tissue-type plasminogen activator (tPA), urinary-type plasminogen activator (uPA) or plasminogen activator inhibitor-1 (PAI-1). Despite the extracellular increase in PAI-1, the net effect of maspin treatment was an increase in plasminogen activation. At physiological levels, maspin did not alter uPA or tPA mRNA levels, in these cells. The increase in pro and active uPA was due to decreased clearance in the presence of maspin for myofibroblasts but not for fibroblasts. The clearance of pro and active tPA was normal in fibroblasts indicating different mechanisms for the increase of these homologous enzymes in the two cell types. Increased generation of plasmin by maspin treated corneal stromal fibroblasts and myofibroblasts led to conversion of plasminogen to active plasmin degradation products and angiostatin-like molecules. This study suggests that extracellular maspin increased pro and active uPA and tPA released by corneal fibroblasts and myofibroblasts on the short time scale of 1–4 h, but by 24 h there was no increase over the levels produced without maspin. This augmentation of plasminogen activator activity increases plasmin activation and angiostatin generation. It further indicates that the effect of maspin on uPA and tPA levels is cell type dependent.     

玻璃体切割术治疗增生性糖尿病视网膜病变中应用曲安奈德的止血作用及其机制

背景 临床发现玻璃体切割术治疗增生性糖尿病视网膜病变(PDR)术中应用曲安奈德(TA)有止血作用,但其机制并不清楚. 目的 探讨玻璃体切割术治疗PDR过程中眼内应用TA止血的作用机制.方法 采用前瞻性研究设计,于2011-2014年纳入在天津医科大学总医院眼科因PDR接受玻璃体切割术且术中眼内应用TA的患者12例12眼,作为TA组,同期因黄斑前膜或黄斑裂孔接受玻璃体切割术且未用TA的患者共32例32眼作为对照组,两组术眼在玻璃体切割术开始时均采集玻璃体样本0.6 ～0.8 ml.采用ELISA法分别测定TA组和对照组患者玻璃体中尿激酶纤溶酶原激活物(u-PA)、组织纤溶酶原激活物(t-PA)及纤溶酶原激活物抑制剂1(AI-1)含量,比较TA组和对照组术前玻璃体样本中上述指标含量的差异.结果 TA组术眼玻璃体中u-PA、t-PA和PAI-1平均质量浓度分别为25.45、127.44和0.42 ng/ml,对照组分别为22.94、142.37和0.27 ng/ml,TA组术眼玻璃体中u-PA平均质量浓度明显高于对照组,差异有统计学意义(Z=-2.268,P＜0.05),TA组和对照组术眼玻璃体中t-PA和PAI-1平均质量浓度的差异均无统计学意义(Z=-0.092、-1.847,均P＞0.05). 结论 PDR患者玻璃体中u-PA平均质量浓度高,易致眼内出血.玻璃体切割术中眼内应用TA可减少或阻止出血其机制可能与t-PA和u-PA平均质量浓度降低而达到降低出血倾向,并通过增加PAI-1质量浓度而发挥止血作用有关.