Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.68 (tissue plasminogen activator)
 11,311 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Contact wide-field specular microscopy was performed on eyes of 16 healthy dogs after tissue plasminogen activator at a concentration of 25 micrograms/100 microliters (group 1, n = 8) or 50 micrograms/100 microliters (group 2, n = 8) was injected into 1 anterior chamber of each dog. The contralateral eye served as a nontreated control. Applanation tonometry was used to measure intraocular pressure in both eyes for up to 168 hours. By use of computerized morphometric analysis and pachymetry, changes from baseline values in endothelial cell density, cell morphologic features, and corneal thickness were evaluated at postinjection hours 24, 48, and 168. Significant mean differences in intraocular pressure were not detected between treated eyes of group-1 dogs and those in group 2 at designated times, or between treated and nontreated eyes of dogs in either group. Mean corneal thickness of treated and nontreated eyes was similar in both groups through postinjection hour 168. Changes in mean percentage of endothelial cell sides were observed only in treated eyes of group-2 dogs, with the mean percentage of hexagons at postinjection hour 168 decreasing by 18%, a decrease that was significantly (P less than 0.05) greater than the decrease in nontreated eyes. The mean percentage of 6-sided cells in treated eyes of group-2 dogs was significantly (P less than 0.05) less than that in treated eyes of group-1 dogs at postinjection hour 168.
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PMID:Effects of intracameral injection of tissue plasminogen activator on corneal endothelium and intraocular pressure in dogs. 162 78

The primary cause of failure in glaucoma filtration surgery is fibroblastic proliferation and subconjunctival fibrosis at the bleb site resulting in decreased aqueous flow. We evaluated New Zealand white rabbits in a masked, placebo controlled pilot study to determine the potential reduction of episcleral fibrosis at the surgical bleb site utilizing 0.3 mls of: balanced salt solution (n = 11); an inert gel delivery vehicle (n = 13); the gel delivery vehicle with incorporated recombinant tissue plasminogen activator (tpa; n = 14), 1 mg/ml. Statistical analysis of computer assisted area measurements from multiple histologic sections demonstrated a significant decrease in episcleral fibrosis in the t-PA group as compared to the two other groups (p less than 0.05). Results from the t-PA group did not demonstrate an effect on intraocular pressure. There was no clinical evidence of toxicity or healing complications in the t-PA group.
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PMID:Subconjunctival high dose plasminogen activator in rabbit filtration surgery. 190 44

We injected 25 micrograms of recombinant tissue plasminogen activator into the anterior chamber or the vitreous cavity in seven aphakic patients for pupillary block caused by a complete fibrin pupillary membrane that formed after vitrectomy with fluid-gas exchange. Progressive fibrin deposition resulted in pupillary block by three days after vitrectomy surgery in six patients, and seven days after vitrectomy in one patient. The pupillary block was associated with increased intraocular pressure in six patients. Tissue plasminogen activator was injected via the corneoscleral limbus in five patients and via the pars plana in two patients. In all patients, injection of tissue plasminogen activator resulted in complete fibrinolysis of the fibrin pupillary membrane within four hours, associated with a deepening of the anterior chamber. In the six patients with increased intraocular pressure at the time of tissue plasminogen activator injection, dissolution of the fibrin membrane was associated with a decrease in pressure. In all patients, intraocular pressure had returned to normal by three days after the injection. No complications were associated with the injection.
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PMID:Treatment of postvitrectomy fibrin pupillary block with tissue plasminogen activator. 250 24

Intraocular fibrin formation following ocular surgery is a potentially binding problem. Current therapy for this postoperative fibrin response is often ineffective. In the rabbit, we developed a quantitative reproducible model for intraocular fibrin deposition. Using this model, we have tested the efficacy of human tissue plasminogen activator (tPA) in promoting intraocular fibrinolysis. Citrated rabbit plasma (0.2 mL) was injected intracamerally following paracentesis, resulting in fibrin clot formation within three hours. The fibrin clots were stable for four days, and then slowly lysed over the next four days. Approximately 24 hours after clot formation, various concentrations of human tPA were injected intracamerally. The time taken for clot lysis was dose dependent, with 1800 IU of tPA producing clot lysis in three hours. Toxicity, as measured by intraocular pressure, corneal thickness, inflammation, or cataract formation, was minimal.
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PMID:Intraocular fibrinolysis with recombinant human tissue plasminogen activator. Experimental treatment in a rabbit model. 311 40

We produced experimental intravitreal fibrin clots in rabbits that had previous gas compression of the vitreous or intact vitreous. Twenty-four hours after production of fibrin, the eyes were injected with 25 micrograms of tissue plasminogen activator or physiologic irrigation solution. In the gas compression group (n = 11), all tissue plasminogen activator-treated eyes cleared within six hours of injection; complete clearing was not seen until six days in the physiologic irrigation solution-treated eyes (n = 9). A similar response was seen in the intact vitreous group. No evidence of toxicity was observed as measured by slit-lamp biomicroscopy, intraocular pressure, corneal thickness, electroretinography, or histopathologic examination.
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PMID:Treatment of experimental intravitreal fibrin with tissue plasminogen activator. 312 May 91

Maintenance of patency of the trabecular meshwork, the major outflow channel of the anterior chamber of the eye, is necessary to prevent an excessive rise in intraocular pressure. Obstruction of flow due to clot formation results in severe glaucoma and damage to the optic nerve. We have found that human trabecular meshwork cells which have been passaged in tissue culture synthesize large amounts of tissue plasminogen activator (t-PA), based on functional, immunologic and molecular weight analysis. Trabecular cells express substantially more t-PA activity than vascular endothelium which produces t-PA for clot dissolution in the systemic circulation. Vascular cells produce excess t-PA inhibitor while trabecular cells make comparatively little. Trabecular meshwork cells are the first normal cell type reported in which the balance between t-PA and inhibitor is weighted towards the activator, indicating that fibrinolysis may be more important than clotting in the anterior chamber of the eye.
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PMID:Tissue plasminogen activator in cultured human trabecular meshwork cells. Predominance of enzyme over plasminogen activator inhibitor. 312 23

In a prospective study performed between June 1992 and March 1994 19 eyes of 19 patients with dense fibrinous pupillary membranes following cataract surgery were treated with intracameral injections of 25 micrograms recombinant tissue plasminogen activator (r-tPA). Injections were performed between the second and twenty-third postoperative day (mean 5.6 +/- 6.9 days). Complete fibrinolysis within one to 4 hours (mean: 3.3 +/- 0.89 hours) was observed in 18 (94.7%) eyes. In one (5.3%) eye fibrinolysis was incomplete despite a second injection. In 2 (10.5%) eyes. No recurrence of a distinct fibrinous membrane was noted which then cleared spontaneously with topical treatment. A small hyphema developed in 2 (10.5%) eyes and intraocular pressure exceeded 25 mmHg in 2 (10.5%) eyes. No increase of keratopathy nor any toxic intraocular side effect of 25 micrograms intracameral r-tPA was observed throughout the study. The intracameral injection of r-tPA clinically proved to safely accelerate the resorption of dense fibrinous membranes following cataract surgery and thus enhance visual recovery minimizing subsequent complications and systemic or subconjunctival anti-inflammatory treatment.
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PMID:The use of recombinant tissue plasminogen activator for intracameral fibrinolysis following cataract surgery. 760 8

Twenty two eyes of 22 cases with severe intraocular fibrin formation after vitrectomy who had been all unresponsive to conventional therapy were treated with tissue plasminogen activator (t-PA), including complicated retinal detachment (14 eyes), intraocular foreign body (3 eyes), vitreous hemorrhage (2 eyes), traumatic cataract (2 eyes) and endophthalmitis (1 eye). The fibrin formation appeared 1-5 days with a mean of 2 days after operation. Of these 22 eyes, fibrin was seen in the pupillary area in 11, in the anterior chamber in 10 eyes and in the vitreous cavity in 1 eye. The initial injection of t-PA was given between the 5th and 15th (mean, 8.6 days) postoperative days after vitrectomy. The t-PA (5-30 micrograms) was injected into the anterior chamber in 21 cases and into the vitreous cavity in 1 case (25 micrograms). Once injection resulted in complete fibrinolysis in 19 of 22 eyes and partial fibrinolysis in 3 eyes, and the complete dissolution with one injection was achieved within 0.5-2.5 hours with a mean of 1 hour. 1 eye required repeated t-PA injection for recurrent fibrin formation and the repeated injection resulted in complete fibrinolysis in this case. The follow-up periods ranged from 1 to 20 months (mean period, 10 months). At the final follow-up examination, the retina was totally attached in 16 of 22 eyes and partially attached and detached in 6. Visual acuity improved in 13 eyes. Complications of t-PA injection included hyphema, elevated intraocular pressure (IOP) and hyphema with elevated IOP in 1 case respectively. Factors affecting the therapeutic effect of t-PA and methods preventing the complications of t-PA injection were discussed.
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PMID:[Treatment of intraocular fibrin formation with tissue plasminogen activator after vitrectomy]. 874 15

The purpose of this study is to investigate the efficacy of tissue plasminogen activator (tPA) in the treatment of total hyphema following ocular trauma or intraocular surgery. Three patients (3 eyes) representing unresolved total hyphema for more than 5 days and uncontrolled high intraocular pressure received intracameral injections of 10 microgram of recombinant tPA. Intracameral tPA injection resulted in complete resolution of hyphema in all 3 eyes. Resolution occurred mostly within 24 to 48 hours after injection. Possible side effects of tPA injection, such as increased intraocular pressure and corneal edema, were not observed. However, 1 eye had vitreous hemorrhage after repeated injections of tPA. Intracameral injection of tPA seems to be a safe and effective method for the treatment of unresolved total hyphema. However, repeated intracameral tPA injections may cause unwanted complications such as vitreous hemorrhage.
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PMID:Treatment of total hyphema with relatively low-dose tissue plasminogen activator. 976 Jun 14

To investigate the role of tissue plasminogen activator (tPA) in retinal damage, tPA-deficient and wild-type mice were employed. Two different retinal neuron insult models were used in the present study. One is an excitotoxin-treated retinal model, created by direct intravitreal injection of glutamate analogs, NMDA or kainic acid (KA), and the other is an ischemia-reperfusion model induced by transient elevation of intraocular pressure. TdT-dUTP terminal nick-end labeling (TUNEL) method was used to examine the retinal cell nuclear damage. The number of TUNEL-positive cells in ganglion cell layer (GCL) and inner nuclear layer (INL) in tPA-deficient mice after low-, but not high-dose NMDA was significantly less compared to wild type. In contrast, neither intravitreal KA or transient ischemia produced significant difference in retinal damage in tPA vs. wild-type mice. These data show that tPA-deficient mice are resistant to retinal damage by intravitreal injection of NMDA, and indicate that tPA plays a role in the retinal cell damage induced by excitotoxins, especially NMDA.
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PMID:Endogenous tissue type plasminogen activator facilitates NMDA-induced retinal damage. 1545 7


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