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微纤溶酶诱导的玻璃体后脱离

Posterior vitreous detachment induced by microplasmin.

作者信息

Gandorfer Arnd, Rohleder Matthias, Sethi Charanjit, Eckle Dominik, Welge-Lüssen Ulrich, Kampik Anselm, Luthert Philip, Charteris David

机构信息

Department of Ophthalmology, University Eye Hospital, Ludwig-Maximilians-University, Munich, Germany.

出版信息

Invest Ophthalmol Vis Sci. 2004 Feb;45(2):641-7. doi: 10.1167/iovs.03-0930.

Abstract

PURPOSE

To demonstrate the efficacy of microplasmin in inducing posterior vitreous detachment (PVD) and to evaluate the human and the feline retina after treatment.

METHODS

Thirteen human donor eyes were injected with 62.5, 125, or 188 micro g microplasmin. The 13 fellow eyes received balanced salt solution. Four of the microplasmin-treated eyes received an additional intravitreal gas injection. After incubation at 37 degrees C for 30 minutes, all globes were placed in 4% paraformaldehyde. Retinal specimens were processed for scanning (SEM) and transmission (TEM) electron microscopy. Five feline eyes were injected with 14.5- or 25- micro g microplasmin. Animals were killed after 1 day, 3 days, or 3 weeks, and retinal specimens were evaluated by electron and confocal microscopy.

RESULTS

In all control eyes, SEM demonstrated the cortical vitreous covering the inner limiting membrane (ILM). Intravitreal injection of 125 or 188 micro g microplasmin resulted in complete PVD. After treatment with 62.5 micro g microplasmin, SEM revealed collagen fibrils covering the ILM. Additional gas injection did not change the dose necessary for PVD. In vivo in cats, 25 micro g microplasmin resulted in complete PVD after 3 days. After 3 weeks, there was complete PVD with both doses of microplasmin. The retina and the ILM were well preserved in all eyes.

CONCLUSIONS

Both after death and in vivo, microplasmin induces a dose-dependent cleavage between the vitreous cortex and the ILM without morphologic alterations of the retina. In the feline eye, there is no cellular response of retinal glial cells or neurons.

摘要

目的

证明微纤溶酶诱导玻璃体后脱离(PVD)的疗效,并评估治疗后人类和猫的视网膜情况。

方法

向13只人类供体眼注射62.5、125或188微克微纤溶酶。13只对侧眼注射平衡盐溶液。4只接受微纤溶酶治疗的眼睛额外进行了玻璃体内气体注射。在37℃孵育30分钟后,将所有眼球置于4%多聚甲醛中。视网膜标本进行扫描电子显微镜(SEM)和透射电子显微镜(TEM)处理。向5只猫眼中注射14.5或25微克微纤溶酶。在1天、3天或3周后处死动物,通过电子显微镜和共聚焦显微镜评估视网膜标本。

结果

在所有对照眼中,SEM显示皮质玻璃体覆盖内界膜(ILM)。玻璃体内注射125或188微克微纤溶酶导致完全性PVD。用62.5微克微纤溶酶治疗后,SEM显示胶原纤维覆盖ILM。额外的气体注射并未改变诱导PVD所需的剂量。在猫体内,25微克微纤溶酶在3天后导致完全性PVD。3周后,两种剂量的微纤溶酶均导致完全性PVD。所有眼中视网膜和ILM均保存良好。

结论

无论是死后还是在体内,微纤溶酶均可诱导玻璃体皮质与ILM之间发生剂量依赖性裂解,且视网膜无形态学改变。在猫眼中,视网膜神经胶质细胞或神经元无细胞反应。

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