Induction of Posterior Vitreous Detachment in Rabbits by Intravitreal Injection of Tissue Plasminogen Activator Following Cryopexy

Hesse, Lutz; Nebeling, Bernd; Schroêder, B.; Heller, Günther; Kroll, P.

doi:10.1006/exer.1999.0772

Cited by 63 publications

(53 citation statements)

References 30 publications

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“…Injection of purified plasmin into the vitreous cavity, 10,13,[18][19][20][21][22] or stimulation of plasmin production in the vitreous by t-PA injection, 23 cryocoagulation followed by t-PA injection, 24 or injection of purified human Degree of residual cortical vitreous of test eyes in groups 1-3 compared with those of control eyes.…”

Section: Discussionmentioning

confidence: 99%

“…It is significant that enzymatic action alone was sufficient to induce PVD without the adjuvant gas bubble injection or cryotherapy necessitated in other studies. 20,24 To assess the cleaving effect of mPlm at the vitreoretinal interface in vivo, we administered three different doses into the vitreous cavity of adult rabbits and observed on 1and 7 days after injection. There was a distinct correlation between the concentration of mPlm and the degree of residual posterior vitreous cortical on 1 day after injection.…”

Section: Enzymatic Vitreolysis W Chen Et Almentioning

confidence: 99%

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Enzymatic vitreolysis with recombinant microplasminogen and tissue plasminogen activator

Huang

et al. 2007

Eye

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Purpose To generate microplasmin (lPlm) using recombinant microplasminogen (lPlg) and recombinant tissue plasminogen activator (rt-PA) before intravitreous injection and to investigate the efficacy of lPlm in inducing posterior vitreous detachment (PVD). Methods Forty-eight female or male New Zealand white rabbits were randomized into three groups. Recombinant human lPlg was incubated with rt-PA with a 200:1 molar ratio at 371C for 40 min. The right eyes of groups 1, 2, and 3, were injected with 0.5, 1.0, and 1.5 U lPlm in 0.1 ml respectively, and 0.1 ml balanced salt solution (BSS) was injected into the left eye as controls. Scanning electron microscopy (SEM), gross specimen examination, B-ultrasonography and optical coherence tomography (OCT) were performed to detect vitreoretinal interface. Results Over eighty percent of recombinant human lPlg could be activated to active lPlm by rt-PA after 40 min incubation. Complete PVD was found at vitreous posterior pole of lPlm-treated eyes without morphological change of retina. Complete PVD of 25, 75, and 87.5% rabbit eyes was induced by 0.5, 1.0 and 1.5 U recombinant lPlm respectively on day 1. The remnants of vitreous cortex at the posterior pole were dependent on the concentration of lPlm. Among the four approaches for detecting PVD, SEM, gross specimen examination, and B-ultrasonography were more effective methods than OCT. Conclusion Intravitreous injection of 1.5 U lPlm can effectively induce complete PVD in rabbit eyes on day 1 without morphological change of retina.

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Section: Discussionmentioning

confidence: 99%

Section: Enzymatic Vitreolysis W Chen Et Almentioning

confidence: 99%

Enzymatic vitreolysis with recombinant microplasminogen and tissue plasminogen activator

Huang

et al. 2007

Eye

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“…In an animal model in rabbit eyes, complete PVD was observed in all eyes treated with 25 mg tissue plasminogen activator. 32 Breakdown of the blood-retinal barrier was necessary to allow plasminogen to enter the vitreous, and this was induced by cryocoagulation. 32 In two clinical pilot studies, 25 mg tissue plasminogen activator was injected into the vitreous of patients with proliferative diabetic retinopathy 15 min before vitrectomy.…”

Section: Hyaluronidasementioning

confidence: 99%

“…32 Breakdown of the blood-retinal barrier was necessary to allow plasminogen to enter the vitreous, and this was induced by cryocoagulation. 32 In two clinical pilot studies, 25 mg tissue plasminogen activator was injected into the vitreous of patients with proliferative diabetic retinopathy 15 min before vitrectomy. 33,34 The results of both studies, however, were contradictory in terms of PVD induction and clinical benefit.…”

Section: Hyaluronidasementioning

confidence: 99%

Enzymatic vitreous disruption

Gandorfer

2008

Eye

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Enzymatic vitreous disruption refers to cleaving the vitreoretinal junction by enzymatic means, thereby inducing posterior vitreous detachment (PVD) and liquefaction of the vitreous gel. Several enzymes have been proposed in this respect, including chondroitinase, hyaluronidase, dispase, and plasmin. In an experimental setting, chondroitinase induced PVD and was helpful in removing epiretinal membranes but no further data have been reported yet.Hyaluronidase liquefies the vitreous as demonstrated in a phase III trial in diabetic patients with vitreous haemorrhage. Dispase induces PVD but also causes inner retinal damage and is now used as an animal model of proliferative vitreoretinopathy. Plasmin has the capability of both PVD induction and liquefaction. However, plasmin is highly unstable and not available for clinical use. Microplasmin (ThromboGenics Ltd, Dublin, Ireland) is a truncated form of human plasmin sharing the same catalytic activity like plasmin. Recombinant microplasmin is under clinical investigation in patients with vitreomacular traction. This review article reports on the current knowledge of enzymatic vitreous disruption and discusses details of the enzyme candidates in basic and clinical research terms.

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“…Not only would this facilitate surgery, but it may prevent disease if performed early in the natural history. Various pharmacologic vitreolysis agents have been tested to date, [21][22][23][24][25][26][27][28][29] but little is known about the exact mechanism of action of these substances, and so far none has met with sufficient success to result in widespread use. Plasmin has been used only in limited series of uncontrolled clinical testing (two published series of nine and seven cases), chondroitinase was used only on 20 patients in a Phase I FDA trial, and hyaluronidase has recently failed a Phase III FDA trial.…”

Section: Pharmacologic Vitreolysismentioning

confidence: 99%

Molecular biology of pharmacologic vitreolysis

Sebag¹

2006

American Journal of Ophthalmology

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Induction of Posterior Vitreous Detachment in Rabbits by Intravitreal Injection of Tissue Plasminogen Activator Following Cryopexy

Cited by 63 publications

References 30 publications

Enzymatic vitreolysis with recombinant microplasminogen and tissue plasminogen activator

Enzymatic vitreolysis with recombinant microplasminogen and tissue plasminogen activator

Enzymatic vitreous disruption

Molecular biology of pharmacologic vitreolysis

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