Background The vitreoretinal traction plays a critical role in the formation of macular hole and cystoid macular edema.Enzymatic vitreolysis has potential in relieving vitreoretinal traction as a simple and less invasive method in comparison with pars plane vitrectomy.ObjectiveThis study is to investigate the effects of plasmin mutant with kringle domains deficiency(Plm△K)on vitreoretinal interface in new Zealand white rabbits.Methods Plm△K was prepared through activating plasminogen mutant with Kringle domains deficiency (Plg△K) by tissue plasminogen activator (tPA).100μL of Plm△K at the dose of 0.5,1.0 and 1.5μmol/min was injected respectively into the vitreous of 48 New Zealand white rabbits and 16 eyes for each dose.B-scan and optical coherence tomography (OCT) were performed to detect the structure variety at the vitreoretinal interface in 1 day and 7 days after injection.The gross anatomy analysis with triamcinolone acetonide fine particle suspension,as well as histopathological examinations by scanning electron microscopy,was performed in the different time points mentioned above.Results Two peptide chains were determined with the relative molecular weight about 26000 and 5000 by the gel imaging analysis of reduced SDS-PAGE.Separation of the posterior vitreous cortex from retina was found after intravitreous injection under the B-scan and OCT.The ultrastructure change of vitreoretinal interface as well as the examination of fine particle suspension by triamcinolone acetonide demonstrated the same outcome.The degree of remnants of vitreous cortex showed the negative correlation with the dosage of Plm△K (r=-0.9516,P=0.048).No significant correlation was found between the degree of remnants of vitreous cortex and the action time(r=-0.720,P=0.470).There was no obvious morphological difference in outer layer of retina between control eyes and Plm△K-treated eyes.No drug-related adverse event was found after intravitreous injection of Plm△K.Conclusion Intravitreous injection of Plm△K alone can induce complete separation of vitreous from retina.This procedure is safe and effective.%目的 研究纤溶酶Kringle区缺失突变体(Plm△K)对兔眼玻璃体视网膜界面的作用.方法 Plm△K由毕赤酵母表达的纤溶酶原Kringle区缺失突变体(Plg△K)经组织纤溶酶原激活剂(tPA)激活产生,并通过发色底物S_(2403)测定其蛋白水解活性.0.5、1.0、1.5μmol/min Plm△K 100μL分别注入16只新西兰白兔的玻璃体腔内,注射后1d、7d在光镜下和扫描电镜下检查,并行大体检查、眼部B型超声和光学相干断层扫描(OCT)检查,观察玻璃体视网膜界面情况.结果 还原性SDS-PAGE凝胶成像分析证实,Plg△K被激活后产生相对分子质量约26000和5000的2条肽链,且具有纤溶酶活性.4种检测结果 均显示Plm△K诱导玻璃体皮质与视网膜的分离.视网膜内表面皮质残留量与Plm△K的剂量呈负相关(r=-0.9516,P=0.048),完全性分离可产生光滑的视网膜内表面.Plm△K注射眼与对照眼的视网膜外层结构均未发现明显的差异.视网膜内表面皮质残留量与药物作用时间有一定的关系,但差异无统计学意义(r=-0.720,P=0.470).对照组和Plm△K处理组间视网膜外层的形态学无明显不同.Plm△K玻璃体注射后未发现视网膜发生药物相关的不良反应.结论 玻璃体腔单独注射Plm△K可有效诱导玻璃体与视网膜的完全性分离,而对外层视网膜结构无明显影响.
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