纤维蛋白溶解酶对视网膜毛细血管周细胞生长调节的研究进展

鉴于纤维蛋白溶解酶(简称纤溶酶)在眼科临床应用广泛,尤其在辅助玻璃体切除术方面效果显著,因此研究纤溶酶对视网膜毛细血管周细胞的影响有助于更好理解糖尿病视网膜病变(DR)的发病机制;为治疗DR提供新途径;为纤溶酶安全有效的在玻璃体内注射辅助玻璃体切除手术提供理论依据.在此综述了纤溶酶对周细胞的生长调节、作用机制及其在眼科临床应用方面的最新研究进展.     

纤维蛋白溶解酶对视网膜毛细血管周细胞生长调节的研究进展

鉴于纤维蛋白溶解酶(简称纤溶酶)在眼科临床应用广泛,尤其在辅助玻璃体切除术方面效果显著,因此研究纤溶酶对视网膜毛细血管周细胞的影响有助于更好理解糖尿病视网膜病变(DR)的发病机制;为治疗DR提供新途径;为纤溶酶安全有效的在玻璃体内注射辅助玻璃体切除手术提供理论依据.在此综述了纤溶酶对周细胞的生长调节、作用机制及其在眼科临床应用方面的最新研究进展.     

纤维蛋白溶解酶对视网膜毛细血管周细胞生长调节的研究进展

鉴于纤维蛋白溶解酶(简称纤溶酶)在眼科临床应用广泛,尤其在辅助玻璃体切除术方面效果显著,因此研究纤溶酶对视网膜毛细血管周细胞的影响有助于更好理解糖尿病视网膜病变(DR)的发病机制;为治疗DR提供新途径;为纤溶酶安全有效的在玻璃体内注射辅助玻璃体切除手术提供理论依据.在此综述了纤溶酶对周细胞的生长调节、作用机制及其在眼科临床应用方面的最新研究进展.     

纤维蛋白溶解酶对视网膜毛细血管周细胞生长调节的研究进展

鉴于纤维蛋白溶解酶(简称纤溶酶)在眼科临床应用广泛,尤其在辅助玻璃体切除术方面效果显著,因此研究纤溶酶对视网膜毛细血管周细胞的影响有助于更好理解糖尿病视网膜病变(DR)的发病机制;为治疗DR提供新途径;为纤溶酶安全有效的在玻璃体内注射辅助玻璃体切除手术提供理论依据.在此综述了纤溶酶对周细胞的生长调节、作用机制及其在眼科临床应用方面的最新研究进展.     

纤维蛋白溶解酶对视网膜毛细血管周细胞生长调节的研究进展

鉴于纤维蛋白溶解酶(简称纤溶酶)在眼科临床应用广泛,尤其在辅助玻璃体切除术方面效果显著,因此研究纤溶酶对视网膜毛细血管周细胞的影响有助于更好理解糖尿病视网膜病变(DR)的发病机制;为治疗DR提供新途径;为纤溶酶安全有效的在玻璃体内注射辅助玻璃体切除手术提供理论依据.在此综述了纤溶酶对周细胞的生长调节、作用机制及其在眼科临床应用方面的最新研究进展.     

纤维蛋白溶解酶对视网膜毛细血管周细胞生长调节的研究进展

鉴于纤维蛋白溶解酶(简称纤溶酶)在眼科临床应用广泛,尤其在辅助玻璃体切除术方面效果显著,因此研究纤溶酶对视网膜毛细血管周细胞的影响有助于更好理解糖尿病视网膜病变(DR)的发病机制;为治疗DR提供新途径;为纤溶酶安全有效的在玻璃体内注射辅助玻璃体切除手术提供理论依据.在此综述了纤溶酶对周细胞的生长调节、作用机制及其在眼科临床应用方面的最新研究进展.     

纤维蛋白溶解酶对视网膜毛细血管周细胞生长调节的研究进展

鉴于纤维蛋白溶解酶(简称纤溶酶)在眼科临床应用广泛,尤其在辅助玻璃体切除术方面效果显著,因此研究纤溶酶对视网膜毛细血管周细胞的影响有助于更好理解糖尿病视网膜病变(DR)的发病机制;为治疗DR提供新途径;为纤溶酶安全有效的在玻璃体内注射辅助玻璃体切除手术提供理论依据.在此综述了纤溶酶对周细胞的生长调节、作用机制及其在眼科临床应用方面的最新研究进展.     

纤维蛋白溶解酶对视网膜毛细血管周细胞生长调节的研究进展

鉴于纤维蛋白溶解酶(简称纤溶酶)在眼科临床应用广泛,尤其在辅助玻璃体切除术方面效果显著,因此研究纤溶酶对视网膜毛细血管周细胞的影响有助于更好理解糖尿病视网膜病变(DR)的发病机制;为治疗DR提供新途径;为纤溶酶安全有效的在玻璃体内注射辅助玻璃体切除手术提供理论依据.在此综述了纤溶酶对周细胞的生长调节、作用机制及其在眼科临床应用方面的最新研究进展.     

纤维蛋白溶解酶对视网膜毛细血管周细胞生长调节的研究进展

鉴于纤维蛋白溶解酶(简称纤溶酶)在眼科临床应用广泛,尤其在辅助玻璃体切除术方面效果显著,因此研究纤溶酶对视网膜毛细血管周细胞的影响有助于更好理解糖尿病视网膜病变(DR)的发病机制;为治疗DR提供新途径;为纤溶酶安全有效的在玻璃体内注射辅助玻璃体切除手术提供理论依据.在此综述了纤溶酶对周细胞的生长调节、作用机制及其在眼科临床应用方面的最新研究进展.     

纤维蛋白溶解酶对视网膜毛细血管周细胞生长调节的研究进展

鉴于纤维蛋白溶解酶(简称纤溶酶)在眼科临床应用广泛,尤其在辅助玻璃体切除术方面效果显著,因此研究纤溶酶对视网膜毛细血管周细胞的影响有助于更好理解糖尿病视网膜病变(DR)的发病机制;为治疗DR提供新途径;为纤溶酶安全有效的在玻璃体内注射辅助玻璃体切除手术提供理论依据.在此综述了纤溶酶对周细胞的生长调节、作用机制及其在眼科临床应用方面的最新研究进展.     

Relationship between vitrectomy and the morphology and function of the retina

Pathological processes in the vitreous will be reflected in the morphology and function of the retina, and these processes can originate from sources outside the vitreous. The purpose of vitreous surgery is to remove the qualitatively and/or morphologically diseased vitreous. Successful vitrectomy will be manifested by an improvement in the structure and/or function of the retina. We have evaluated the morphology of the vitreoretinal interface, and the function of the retina before and after vitreous surgery. Plasmin-assisted vitrectomy was used in some cases to remove the diseased vitreous more efficiently and less invasively. The effect of this procedure was assessed by examining the morphology and function of the retina. First, the relationship between the qualitative and structural abnormality of the vitreous in macular diseases was studied. In aphakic/pseudophakic eyes with cystoid macular edema, there was a depression of retinal function over the entire retina which may have been caused by chemical mediators released into the vitreous. These mediators may have been produced by inflammation in the anterior segment of the eye. In eyes with an idiopathic macular hole, optical coherence tomographic (OCT) images suggested that the progression of the macular hole might depend on a balance between foveal adhesion and the posterior vitreous. Second, the efficacy, surgical damage, and limitations of vitreous surgery were investigated. The recovery of macular function was assessed by focal macular electroretinograms (FMERGs) after vitrectomy for epiretinal membrane, choroidal neovascularization, and diabetic macular edema. The concurrent examination by optical coherence tomography (OCT) suggested that a decrease in retinal thickness contributed to the functional recovery. Macular functional recovery was delayed and limited after macular translocation, diabetic macular edema, and internal limiting membrane peeling. Third, we studied the effect of plasmin-assisted vitrectomy on the retina. The plasmin was used to remove the vitreous more completely and less invasively. In rabbits, ERG, OCT, and histological examinations demonstrated that the use of commercially-available plasmin at a concentration used on human patients resulted in temporary adverse effects on the retina. For human patients, we purified the plasmin from the patients' serum at the Nagoya University Hospital and the activity was about the same as in previous reports. The purified plasmin was approved by our hospital's institutional review board, and written informed consent was obtained from each patient. Patients with macular edema, idiopathic macular hole, and epiretinal membrane without posterior detachment underwent plasmin-assisted vitrectomy and were evaluated morphologically and electrophysiologically. The efficacy of the plasmin in separating the vitreo-retinal interface was demonstrated by an occasional spontaneous posterior vitreous detachment with or without core vitrectomy, and the presence of less vitreous cortex attached to the internal limiting membrane that was removed during vitrectomy. This was the first histological demonstration of the effectiveness of plasmin in the living eye. Full-field ERGs before and after surgery demonstrated clear evidence that no alteration of retinal functional had occurred, although we did detect a possible osmotic effect by an increase in OCT-determined retinal thickness by the high-molecular weight autologous plasmin. In future studies, the proper concentration and reaction time for each condition of the vitreous should be determined. In conclusion, the pathophysiology of the vitreous should reflect the retinal function. The recovery of the structure of the retina is important for the recovery of retinal function. This should always be the primary goal of surgeons who perform quality surgery.     

Plasmin in subretinal fluid

Proteolytic activity was studied in subretinal fluid from 56 eyes with rhegmatogenous retinal detachment without vitreous or subretinal hemorrhage. Active plasmin (1.0-15.2 micrograms/ml) was found in 33 eyes and plasmin-inhibitor complexes in 3 eyes. Plasmin was detected more often in large detachments, but there was no clear correlation with the duration of the detachment or characteristics of the holes in the retina. It seems possible that plasmin in subretinal fluid may enhance release of cells from the pigment epithelium by degrading the extracellular matrix and contribute to the development of proliferative vitreoretinopathy.     

Intravitreale Injektionen

Since 1996 acute subretinal hemorrhages have been treated by intravitreal injections. Large proteins injected into the vitreous cavity can cross the retina as well as the underlying retinal pigment epithelium. After intravitreal injection of tissue plasminogen activator (TPA), plasminogen, which is part of a subretinal clot, is converted to plasmin in the presence of fibrin. Plasmin is a relatively unspecific protease that liquefies a formed fibrin clot. Simultaneous intravitreal injection causes an inferior displacement of the liquefied hemorrhage. Beside mechanical effects on subretinal clots plasmin inhibits choroidal neovascularization by hydrolysis of the extracellular matrix as well as growth factors. After successful displacement of a subretinal hemorrhage an additional anti-VEGF (vascular endothelial growth factor) therapy is required.     

Ultrastructure of the vitreoretinal interface following plasmin assisted vitrectomy

AIMS: To investigate the ultrastructure of the vitreoretinal interface following plasmin induced posterior vitreous detachment. METHODS: Plasmin (1 or 2 U/0.1 ml) was injected into the vitreous cavity of 24 eyes of freshly slaughtered pigs. The 24 fellow eyes received calcium-free and magnesium-free PBS and served as a control. After incubation at 37 degrees C for 30 and 60 minutes, the globes were placed in fixative and hemisected. Specimens for light, scanning, and transmission electron microscopy were obtained from the posterior pole, the equator, and the vitreous base using a corneal trephine. RESULTS: All plasmin treated eyes showed posterior vitreous detachment. However, the inner limiting membrane (ILM) was covered by remnants of cortical vitreous at the posterior pole and at the equator. There was a direct correlation between the concentration and exposure times of plasmin and the degree of vitreoretinal separation. Eyes exposed to 1 U plasmin for 30 minutes had a dense network of residual collagen fibrils while those exposed to 1 U plasmin for 60 minutes had only sparse collagen fibrils covering the ILM. Eyes treated with 2 U plasmin for 60 minutes had a smooth retinal surface, consistent with a bare ILM. At the vitreous base there was no vitreoretinal separation. In all control eyes the vitreous cortex was completely attached to the retina. There was no evidence of retinal damage in any plasmin treated eye. CONCLUSION: Plasmin induces a cleavage between the vitreous cortex and the ILM without morphological changes to the retina. In contrast with previous reports, plasmin produces a smooth retinal surface and additional surgery is not required in this experimental setting. The degree of vitreoretinal separation depends on the concentration and length of exposure to plasmin.     

Tissue Plasminogen Activator in the Treatment of Vitreoretinal Diseases

Tissue plasminogen activator (tPA) is a thrombolytic agent that activates plasminogen into plasmin almost exclusively in the presence of fibrin. Intraocular injection of tPA has been proposed for the treatment of vitreoretinal diseases, such as vitreous hemorrhage, postvitrectomy fibrin formation. submacular hemorrhage, retinal vascular occlusive disorders, suprachoroidal hemorrhage and endophthalmitis. Currently, intraocular tPA is only used in the treatment of postvitrectomy fibrin formation and submacular hemorrhage. For other indications, tPA has not been shown to be safe or effective. This article reviews the use of tPA in the treatment of vitreoretinal disorders     

Tissue plasminogen activator in the treatment of vitreoretinal diseases

Tissue plasminogen activator (tPA) is a thrombolytic agent that activates plasminogen into plasmin almost exclusively in the presence of fibrin. Intraocular injection of tPA has been proposed for the treatment of vitreoretinal diseases, such as vitreous hemorrhage, postvitrectomy fibrin formation, submacular hemorrhage, retinal vascular occlusive disorders, suprachoroidal hemorrhage and endophthalmitis. Currently, intraocular tPA is only used in the treatment of postvitrectomy fibrin formation and submacular hemorrhage. For other indications, tPA has not been shown to be safe or effective. This article reviews the use of tPA in the treatment of vitreoretinal disorders.     

Management of postvitrectomy diabetic vitreous hemorrhage with tissue plasminogen activator (t-PA) and volume homeostatic fluid-fluid exchanger.

The incidence of recurrent vitreous hemorrhage of proliferative diabetic retinopathy following posterior vitrectomy ranges from 29% to 75% in reported series. Fluid-gas exchange and vitreous cavity lavage are the popular methods of treating this kind of recurrent hemorrhage. The fluid-gas exchange cannot offer clear vision immediately after the procedure. To improve the function of the classic vitreous cavity lavage, we designed a volume homeostatic fluid-fluid exchanger - Chen's I/A device. Tissue plasminogen activator (t-PA) is a protease that preferentially converts fibrin-bound plasminogen to the active proteolytic enzyme, plasmin. It has been clinically and experimentally proven effective in lysis of postvitrectomy blood clot and fibrin formation. When the blood clot is formed in the vitreous cavity, intravitreal injection of t-PA can convert plasminogen to plasmin and remove the clot. From July 1999 to January 2000, ten eyes of postvitrectomy diabetic vitreous hemorrhage (PDVH) were collected. In each case, 4 days after intravitreal injection (IVI) of t-PA (30 microg), vitreous cavity lavage was performed with Chen's I/A device. Of these cases, 8 eyes (80%) experienced an immediate clearing of the vitreous cavity. Early complications included anterior hyaloid fibrovascular proliferation (2 eyes) and postoperative intraocular pressure elevation (3 eyes). On the basis of the results of this study, our conclusion is that volume homeostatic vitreous cavity lavage, combined with intravitreal injection of t-PA, is an excellent method for treatment of postvitrectomy diabetic vitreous hemorrhage but, in cases of PDVH with iris rubeosis, the advantage of this procedure is uncertain.     

Causes of vitreous hemorrhage

It is often a challenge for the ophthalmologist to find the underlying cause of a vitreous hemorrhage. Unless clinical signs clearly point in another direction, the first suspicion should always be a posterior vitreous detachment causing a retinal tear. The other two major causes, diabetic retinopathy and retinal vein occlusion, remain common complications in spite of recent years' improvement in retinal treatment. Macroaneurysm is one of the most often overlooked causes of vitreous hemorrhage. An ocular tumor sometimes presents with a vitreous hemorrhage. In all cases of dense vitreous hemorrhages, the use of diagnostic ultrasonography is mandatory.     

Posterior vitreous detachment induced by injection of plasmin and sulfur hexafluoride in the rabbit vitreous

PURPOSE: To investigate whether an injection of plasmin and sulfur hexafluoride (SF6) can induce posterior vitreous detachment (PVD) without vitrectomy. METHODS: One eye each of 15 New Zealand white rabbits was assigned to one of three groups. Eyes in group 1 received a vitreous injection of 1 unit of human plasmin (0.1 mL reconstituted in balanced salt solution) and 0.5 mL of SF6; eyes in group 2 received a vitreous injection of plasmin alone; eyes in group 3 received a vitreous injection of SF6 alone. Seven days after injection, all animals were monitored electroretinographically and killed, and the eyes were enucleated. After fixation, scanning electron microscopy was performed. RESULTS: In group 1 eyes, the retinal surface was smooth except for the vitreous base, which showed complete separation of the vitreous cortex from the retina, indicating PVD. In group 2 and 3 eyes, sparse collagen fibers remained on the retinal surface. CONCLUSION: Vitreous injection of plasmin combined with SF6 can induce PVD without vitrectomy.     

引起玻璃体出血的视网膜裂孔激光治疗

目的探讨激光治疗伴玻璃体出血的视网膜裂孔的疗效。方法对26例伴玻璃体出血的视网膜裂孔的病例在表麻下行氩离子激光治疗,评估疗效。结果除1例因玻璃体出血量较多且裂孔周围浅脱离范围较大,激光治疗失败外,其余病人均获得满意的疗效,视力提高、玻璃体出血吸收、视网膜裂孔封闭良好。结论氩离子激光是治疗伴玻璃体出血的视网膜裂孔的有效方法。