22 results on '"Vitreous Body blood supply"'
Search Results
2. Studies on the pathogenesis of avascular retina and neovascularization into the vitreous in peripheral severe retinopathy of prematurity (an american ophthalmological society thesis).
- Author
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Hartnett ME
- Subjects
- Animals, Animals, Newborn growth & development, Animals, Newborn metabolism, Cryotherapy, Disease Models, Animal, Genetic Predisposition to Disease, Laser Therapy, Lipocalin 1 genetics, Neovascularization, Pathologic metabolism, Protein Isoforms, RNA, Messenger metabolism, Rats, Rats, Sprague-Dawley, Retina metabolism, Retinal Diseases metabolism, Retinal Diseases therapy, Severity of Illness Index, Up-Regulation, Vascular Endothelial Growth Factor A genetics, Vascular Endothelial Growth Factor A metabolism, Neovascularization, Pathologic etiology, Premature Birth, Retinal Diseases complications, Retinal Diseases pathology, Retinal Vessels abnormalities, Vitreous Body blood supply
- Abstract
Purpose: To study vascular endothelial growth factor (VEGF) regulation in the development of intravitreous neovascularization and peripheral avascular retina in peripheral severe retinopathy of prematurity (ROP)., Methods: The rat 50/10 model of ROP mimics zone II, stage 3 severe ROP and recreates fluctuations in transcutaneous oxygen levels in preterm infants. On postnatal (p) day ages p0, p8, p11-p14, and p18, retinas from the model or room-air (RA) age-matched pups were analyzed for mRNA of VEGF splice variants and receptors using real-time polymerase chain reaction or VEGF protein using enzyme-linked immunosorbent assay., Results: On p14, when retinas were only 70% vascularized in the model but fully vascularized in RA, VEGF₁₆₄ expression was threefold greater in the model compared to RA. On p18, intravitreous neovascularization was associated with a 5-fold increase in VEGF₁₆₄ mRNA in the model compared to RA. By analysis of variance, VEGF₁₆₄ and VEGFR2 mRNAs were up-regulated in association with increasing developmental age (P<.0001 for both comparisons) or exposure to the model compared to RA (P<.0001 and P=.0247, respectively), whereas increasing developmental age was associated only with up-regulated VEGF₁₂₀ (P=.0006), VEGF₁₈₈ (P=.0256), and VEGFR1 (P<.0001) mRNAs. VEGF protein increased significantly in the model and on p14 and p18 compared to RA (P<.0001)., Conclusions: The model mimics contemporary severe ROP in the United States unlike other models of oxygen-induced retinopathy. Compared to RA retinas, VEGF significantly increased in association with avascular retina and intravitreous neovascularization. A hypothesis is proposed that VEGF up-regulation plays a role in the development of both important features.
- Published
- 2010
3. Prospects for treatment of pediatric vitreoretinal diseases with vascular endothelial growth factor inhibition.
- Author
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Lin KL, Hirose T, Kroll AJ, Lou PL, and Ryan EA
- Subjects
- Angiogenesis Inhibitors therapeutic use, Antibodies, Monoclonal therapeutic use, Antibodies, Monoclonal, Humanized, Bevacizumab, Eye blood supply, Humans, Incontinentia Pigmenti complications, Infant, Infant, Newborn, Male, Neovascularization, Pathologic drug therapy, Neovascularization, Pathologic etiology, Preoperative Care, Retinal Detachment etiology, Retinal Detachment surgery, Retinal Vessels abnormalities, Retinopathy of Prematurity drug therapy, Eye Diseases drug therapy, Retinal Diseases drug therapy, Vascular Endothelial Growth Factor A antagonists & inhibitors, Vitreous Body blood supply
- Abstract
While angiogenesis inhibitors are already widely used to treat retinal disease in adults, only limited reports are currently available for the use of anti-VEGF in pediatric vitreoretinal diseases such as retinopathy of prematurity, Coats' disease, familial exudative vitreoretinopathy and retinopathy of incontinentia pigmenti. The limited trials of anti-VEGF therapy for pediatric vitreoretinal diseases are promising, although more extensive controlled trials will be needed to confirm their safety and efficacy. This paper will examine the current evidence for use of anti-VEGF therapy in a number of pediatric vitreoretinal disorders and describe a case of anti-VEGF therapy in retinopathy of incontinentia pigmenti.
- Published
- 2009
- Full Text
- View/download PDF
4. Neutralizing antibody to VEGF reduces intravitreous neovascularization and may not interfere with ongoing intraretinal vascularization in a rat model of retinopathy of prematurity.
- Author
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Geisen P, Peterson LJ, Martiniuk D, Uppal A, Saito Y, and Hartnett ME
- Subjects
- Animals, Animals, Newborn, Blotting, Western, Disease Models, Animal, Lectins metabolism, Neutralization Tests, Oxygen, Phosphorylation drug effects, Rats, Rats, Sprague-Dawley, Retina drug effects, Retina metabolism, Retina pathology, Retinal Diseases chemically induced, Time Factors, Vascular Endothelial Growth Factor Receptor-2 metabolism, Vitreous Body drug effects, Antibodies pharmacology, Retinal Diseases immunology, Retinal Diseases pathology, Retinal Neovascularization pathology, Vascular Endothelial Growth Factor A immunology, Vitreous Body blood supply
- Abstract
Purpose: To study the effects of a neutralizing antibody to vascular endothelial growth factor (VEGF), given as an intravitreous injection, on intravitreous neovascularization (IVNV) and ongoing vascular development of avascular retina in a rat model relevant to human retinopathy of prematurity., Methods: Newborn Sprague-Dawley rats were exposed to oxygen fluctuations alternating between 50% O(2) and 10% O(2) every 24 h. At postnatal day (p)12, rat pups received intravitreous injections of a neutralizing antibody to VEGF or control nonimmune rat IgG in one eye and were returned to oxygen cycling until p14, at which time they were placed into room air. At p18 (time of maximal IVNV) or p25 (time point in regression), animals were sacrificed. Their retinas were dissected, flat mounted, and stained with Alexa-isolectin for fluorescence microscopy. IVNV was measured as number of clock hours involved in injected VEGF antibody and control eyes. Mean clock hours of IVNV, avascular/total retinal areas and capillary densities within vascularized retinas were determined in injected eyes of control and treatment groups. Mean clock hours of IVNV in fellow noninjected eyes from control and treatment groups were analyzed by Student's t-tests to assess possible crossover effects from systemic absorption of antibody. Eyes from p13 rat pups were sectioned for immunohistochemistry or analyzed for VEGF receptor 2 (VEGFR2) phosphorylation by western blot. Free retinal VEGF at p13, one day following injections, was measured by ELISA., Results: Neutralizing antibody to VEGF at 25 ng and 50 ng caused a modest but significant inhibition of IVNV compared to IgG injected controls at p18, but only the 50 ng dose decreased IVNV compared to control at p25 (one-way ANOVA p=0.003; posthoc Bonferroni t-test p=0.003). Neither dose caused a significant difference in avascular/total retinal area at p18 compared to control. However, at p25, the 50 ng dose caused a significant reduction in avascular/total retinal area compared to the 25 ng dose (ANOVA p=0.038; posthoc Student's t-test p=0.038). There was no difference in avascular/total retinal area between IgG and the 25 ng dose. At p13, qualitative analysis of immunohistochemical sections of retina showed the 50 ng dose of VEGF antibody reduced VEGFR2 phosphorylation within the retina and around blood vessels. Also at p13, there was a significant increase in free intraretinal VEGF protein in eyes that had been treated with 50 ng dose of VEGF antibody compared to IgG injected control (Student's t-test p=0.042). There were no differences in capillary densities in the vascularized retinas between eyes injected with the 50 ng dose of VEGF antibody and IgG control. There was also no difference in weight gain between treated and control groups., Conclusions: Neutralizing antibody to VEGF at a 50 ng dose caused a significant and sustained reduction in IVNV without interfering with ongoing retinal vascularization in a rat model of ROP, whereas a lower dose of antibody did not. These data also suggest that compensatory regulatory mechanisms may lead to increased VEGF concentration after intravitreous injection of a neutralizing antibody to VEGF. Further study is necessary for safety and for determination of drug dose of VEGF antibody, since dose of treatment appears important and may vary among infants with severe ROP. In this study, survival of already developed retinal capillaries did not appear affected. Neutralizing VEGF by an intravitreous injection of antibody may offer a treatment consideration for severe ROP, which fails current standard of care management.
- Published
- 2008
5. COX-2 protects against thrombosis of the retinal vasculature in a mouse model of proliferative retinopathy.
- Author
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Cryan LM, Pidgeon GP, Fitzgerald DJ, and O'Brien CJ
- Subjects
- Animals, Animals, Newborn, Blood Platelets pathology, Cell Nucleus ultrastructure, Cyclooxygenase 1 deficiency, Endothelial Cells pathology, Fibrinogen metabolism, Immunohistochemistry, Lectins, Mice, Mice, Inbred C57BL, Mice, Knockout, Oxygen, Prostaglandins biosynthesis, Regional Blood Flow, Retina pathology, Retinal Diseases chemically induced, Retinal Diseases pathology, Retinal Vessels metabolism, Retinal Vessels physiopathology, Staining and Labeling, Vitreous Body blood supply, Vitreous Body pathology, Cyclooxygenase 2 metabolism, Retinal Diseases metabolism, Retinal Diseases prevention & control, Thrombosis prevention & control
- Abstract
Purpose: Cyclooxygenases (COX-1 and COX-2) and prostaglandins regulate angiogenesis in several settings, including cancer and ischemia. In the eye, both selective inhibitors of COX-2 and nonselective COX inhibitors are reported to suppress ischemia-related retinal angiogenesis. Such studies however, may be confounded by the nonspecific effects of inhibitors., Methods: Mice lacking either the COX-1 (COX-1(-/-)) or COX-2 isoform (COX-2(-/-)) were employed in a model of oxygen-induced retinopathy. Vascular responses were examined by histology, isolectin B4 staining of the abluminal endothelium, and retinal fluorescein angiography., Results: There was an increase in intravitreal endothelial nuclei in hyperoxia-treated mice compared to normoxic controls irrespective of the genotype. Quantitative analysis of fluorescein-perfused and isolectin B4-stained retinal angiograms at postnatal day 18 (P18) revealed similar global levels of neovascular tufts in hyperoxia-treated wild-type, COX-1(-/-), and COX-2(-/-) mice. However, hyperoxia-treated COX-2(-/-) mice had increased areas of retinal nonperfusion (29.2+/-1.9 compared to 16.3+/-2.7; n=6; p<0.001). COX-1 disruption had no effect (15.6+/-2.6; n=8). Platelet deposition within retinal vessels was increased in hyperoxia-treated COX-2(-/-) mice (p<0.05)., Conclusions: Genetic disruption of a single COX isoform is not sufficient to prevent oxygen-induced retinopathy. COX-2 protects retinal vessels from thrombosis, limiting the area of retinal nonperfusion in oxygen-induced retinopathy.
- Published
- 2006
6. Persistence of fetal vasculature in a patient with Knobloch syndrome: potential role for endostatin in fetal vascular remodeling of the eye.
- Author
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Duh EJ, Yao YG, Dagli M, and Goldberg MF
- Subjects
- Child, Collagen Type XVIII genetics, DNA Mutational Analysis, Enzyme-Linked Immunosorbent Assay, Fluorescein Angiography, Humans, Hyperplasia, Male, Mutation, Myopia genetics, Syndrome, Vitreous Body pathology, Cerebellum abnormalities, Choroid Diseases genetics, Encephalocele genetics, Endostatins blood, Eye Diseases, Hereditary genetics, Retinal Diseases genetics, Vitreous Body abnormalities, Vitreous Body blood supply
- Abstract
Objective: To report a child with Knobloch syndrome (KS) with features of persistent fetal vasculature (PFV) and to discuss the possible role of endostatin in vascular remodeling of the fetal eye., Design: Case report with enzyme-linked immunosorbent assay (ELISA) analysis of serum endostatin., Main Outcome Measures: Ocular examination, fluorescein angiography, echography, ELISA analysis of serum endostatin, and typing for pathogenic mutations in COL18A1., Results: Slit-lamp examination in the left eye disclosed numerous findings of PFV, including an extensive persistent pupillary membrane, scarcity of iris crypts, and pigmented epicapsular stellate remnants on the anterior lens surface. Dilated fundus examination revealed a total posterior vitreous detachment, despite the young age of the patient, with numerous white intragel opacities that were compatible with remnants of the vasa hyaloidea propria. The fundus had a tesselated appearance with angiographically visible large choroidal vessels. There was a retinochoroidal staphyloma inferotemporal to the optic disc. There were no retinal vessels visible temporally, and there was no macular differentiation or foveal pit. Competitive ELISA analysis disclosed no detectable serum endostatin. None of the 8 reported pathogenic mutations in the COL18A1 gene was found in the patient., Conclusions: Persistent fetal vasculature may be a clinical and important manifestation in some patients with KS and can be explained by a deficiency in endostatin. Endostatin deficiency may result in reduced or delayed regression of fetal blood vessels in the eye (including the intravitreal compartment), thereby resulting in incomplete development of the normal vasculature in the retina. Our typing results for the reported COL18A1 mutations confirm the genetic heterogeneity of KS.
- Published
- 2004
- Full Text
- View/download PDF
7. Are congenital prepapillary arterial loops changeable?
- Author
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Ding PC and Chen MT
- Subjects
- Adolescent, Fluorescein Angiography, Fundus Oculi, Humans, Male, Retinal Diseases pathology, Vitreous Body blood supply, Eye Abnormalities pathology, Optic Disk blood supply, Retinal Artery abnormalities, Retinal Diseases congenital
- Published
- 2001
- Full Text
- View/download PDF
8. Prepapillary arterial loops.
- Author
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Ding PC and Chen MT
- Subjects
- Adult, Child, Female, Fluorescein Angiography, Fundus Oculi, Humans, Male, Retinal Diseases diagnosis, Eye Abnormalities diagnosis, Optic Disk blood supply, Retinal Artery abnormalities, Retinal Diseases congenital, Vitreous Body blood supply
- Published
- 1999
- Full Text
- View/download PDF
9. Coats'-like response in pars planitis.
- Author
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Suh DW, Pulido JS, Jampol LM, Chong LP, and Thomas M
- Subjects
- Adult, Female, Humans, Macular Edema etiology, Neovascularization, Pathologic etiology, Retinal Neovascularization etiology, Visual Acuity, Vitreous Body blood supply, Vitreous Hemorrhage etiology, Pars Planitis complications, Retinal Diseases etiology
- Published
- 1999
- Full Text
- View/download PDF
10. Coats' disease and persistent hyperplastic primary vitreous. Role of MR imaging and CT.
- Author
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Edward DP, Mafee MF, Garcia-Valenzuela E, and Weiss RA
- Subjects
- Aneurysm diagnostic imaging, Ciliary Body diagnostic imaging, Ciliary Body pathology, Contrast Media, Diagnosis, Differential, Humans, Hyperplasia, Image Enhancement, Infant, Microphthalmos diagnosis, Microphthalmos diagnostic imaging, Radiographic Image Enhancement, Retinal Detachment diagnostic imaging, Retinal Diseases diagnostic imaging, Retinal Neoplasms diagnosis, Retinal Vessels diagnostic imaging, Retinoblastoma diagnosis, Telangiectasis diagnostic imaging, Vitreous Body blood supply, Vitreous Body diagnostic imaging, Aneurysm diagnosis, Magnetic Resonance Imaging, Retinal Detachment diagnosis, Retinal Diseases diagnosis, Retinal Vessels pathology, Telangiectasis diagnosis, Tomography, X-Ray Computed, Vitreous Body pathology
- Abstract
Coats' disease is an idiopathic disorder in which telangiectatic and aneurysmal retinal vessels leak a lipoproteinaceous exudate, with consequent bullous retinal detachment. It is a diagnostic challenge, and CT and MR imaging provide valuable information to differentiate it from other pathologies, particularly from retinoblastoma. Typical, advanced Coats' disease shows on CT a denser substance posterior to the vitreous, which on MR is hyperintense on all pulse sequences. Contrast administration on both CT and MR might give slight linear enhancement at the boundary between vitreous and exudation. Persistent hyperplastic primary vitreous (PHPV) is a unilateral disorder in a microphthalmic eye, seen in full-term infants. PHPV rarely is bilateral in patients with Norrie's disease, Warburg syndrome, or patients with retinal dysplasia. Persistent fetal vasculature leads to fibrosis, resulting in elongation of the ciliary processes, retinal detachment, and spontaneous cataracts. The CT appearance in the disorder is quite variable; however, MR imaging may be superior in demonstrating the enhancing retrolental mass and the elongated ciliary processes.
- Published
- 1998
- Full Text
- View/download PDF
11. Diagnostic and therapeutic challenges.
- Author
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Schatz H
- Subjects
- Child, Fibrosis, Fluorescein Angiography, Fundus Oculi, Humans, Male, Visual Acuity, Vitreous Body blood supply, Retinal Diseases diagnosis, Retinal Vessels pathology
- Published
- 1996
- Full Text
- View/download PDF
12. Oxygen-induced retinopathy: ultrastructure of vitreous new vessels in the kitten model.
- Author
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Gole GA, Browning J, and Elts SM
- Subjects
- Animals, Capillary Permeability, Cats, Disease Models, Animal, Endothelium, Vascular ultrastructure, Neovascularization, Pathologic pathology, Oxygen, Perfusion, Retinal Diseases chemically induced, Retinal Diseases physiopathology, Vitreous Body ultrastructure, Retinal Diseases pathology, Vitreous Body blood supply
- Abstract
Oxygen-induced retinopathy was produced by exposing 3-day-old kittens to 80% oxygen between 60 and 105 hours. They were then allowed to survive in room air until day 15, 21 or 28 when they were sacrificed after perfusion with colloidal carbon. Specimens were prepared for transmission electron microscopy. Ninety separate vitreous capillaries from oxygen-treated animals were examined. A total of 235 intercellular junctions were examined, 116 of them from the 15-day old animals. In the 15-day old animals, five junctions of 116 were open and the remainder were tight. No open junctions were seen in 21- or 28-day-old animals. In one capillary from a 15-day animal, fenestrated endothelium was seen in an aberrant, intraluminal loop of endothelium which formed no part of the blood/tissue barrier. The wall thickness of the vitreous new vessels seemed to decrease and the number of vesicles and vacuoles appeared to increase with increasing age. The basement membrane of the vitreous new vessels was scanty. In some sections, cells, presumably macrophages, were seen outside the new vessels. It is concluded that the increased permeability of the vitreous new vessels in 15-day-old animals can be explained by, and is possibly totally due to, the presence of open endothelial junctions.
- Published
- 1990
- Full Text
- View/download PDF
13. [Pathological studies on the retinopathy of prematurity (ROP)--comparison between still-born and premature babies].
- Author
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Okuda T, Yamamoto M, and Itoh H
- Subjects
- Capillaries pathology, Female, Humans, Immunoenzyme Techniques, Infant, Newborn, Male, Pregnancy, Vitreous Body blood supply, Eye pathology, Fetal Death pathology, Infant, Premature, Retinal Diseases pathology
- Published
- 1985
14. Management of retinal branch vein occlusion: the role of argon laser photocoagulation.
- Author
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Kelley JS, Patz A, and Schatz H
- Subjects
- Capillary Permeability, Edema complications, Edema surgery, Fluorescein Angiography, Humans, Macula Lutea blood supply, Middle Aged, Retinal Diseases blood, Retinal Diseases classification, Retinal Diseases complications, Retinal Diseases diagnosis, Retinal Hemorrhage complications, Retinal Hemorrhage surgery, Vision, Ocular, Visual Acuity, Vitreous Body blood supply, Argon, Laser Therapy, Lasers, Retinal Diseases surgery, Retinal Vein surgery
- Published
- 1974
15. Chorioretinal and choriovitreal neovascularization. Their presence after photocoagulation of proliferative sickle cell retinopathy.
- Author
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Dizon-Moore RV, Jampol LM, and Goldberg MF
- Subjects
- Adult, Choroid pathology, Humans, Light Coagulation, Middle Aged, Postoperative Complications, Retinal Diseases etiology, Retinal Vessels, Vitreous Body blood supply, Anemia, Sickle Cell complications, Choroid blood supply, Neovascularization, Pathologic, Retinal Diseases surgery
- Abstract
Delayed development of choroidally fed neovascularization represents a potentially serious complication of feeder vessel photocoagulation of proliferative sickle cell retinopathy (PSR). Of the 53 photocoagulated eyes, choroidally fed neovascularization developed in 21 within one month to seven years (mean, 32.8 months). This complication appeared in eyes treated with argon laser and xenon arc. In 11, neovascular tissue remained flat in the chorioretinal scar (chorioretinal neovascularization), but in ten, the vessels grew into the vitreous (choriovitreal neovascularization). In many cases of chorioretinal neovascularization, the only subsequent complication was local vitreous hemorrhage. Visual acuities remained near normal. The development of choriovitreal neovascularization was associated with vitreous hemorrhages or retinal detachment in six of ten cases. Final visual acuities, however, were 20/50 or better in nine. Photocoagulation in some cases converted chorioretinal neovascularization to choriovitreal neovascularization or seemed to stimulate further growth of choriovitreal neovascularization. We now recommend no treatment for most cases of choroidally fed neovascularization. Photocoagulation techniques for PSR should attempt to minimize the development of choroidally fed neovascularization.
- Published
- 1981
- Full Text
- View/download PDF
16. Components of vitreous-soluble proteins: effect of hyperoxia and age.
- Author
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Chen CH and Patz A
- Subjects
- Age Factors, Animals, Blood Vessels growth & development, Diabetic Retinopathy etiology, Dogs, Female, Hyperbaric Oxygenation, Male, Solubility, Vitreous Body blood supply, Oxygen Consumption, Proteins metabolism, Retinal Diseases metabolism, Vitreous Body metabolism
- Abstract
In young puppies, the retina, which is incompletely vascularized at birth becomes fully vascularized at approximately four weeks of age. During this period of vessel growth the total content of vitreous-soluble protein was found closely associated with the rate of retinal vessel growth. As vascularization progressed toward completion, the protein originally present at birth decreased to a negligible or undetected amount. Intravitreal neovascularization was produced in young puppies by exposure to 85 per cent oxygen for four days, then removal to room air. This form of neovascularization resembles closely that observed in human proliferative diabetic retinopathy. The oxygen treatment, which initially produced retinal capillary closure, then neovascularization, was associated with a retention of vitreous-soluble protein at a high level for several days. The results raise the possibility that the vitreous protein(s) may be fundamentally involved in the process of normal vascularization of the retina and in retinal neovascularization.
- Published
- 1976
17. Focal photocoagulation of retinovitreal neovascularization.
- Author
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L'esperance FA Jr
- Subjects
- Argon, Fluorescein Angiography, Humans, Optic Disk blood supply, Retinal Diseases classification, Retinal Diseases pathology, Vitreous Body pathology, Laser Therapy, Lasers methods, Retinal Diseases surgery, Retinal Vessels surgery, Vitreous Body blood supply
- Published
- 1976
- Full Text
- View/download PDF
18. Choroido-vitreal neovascularization after argon laser photocoagulation.
- Author
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Galinos SO, Asdourian GK, Woolf MB, Goldberg MF, and Busse BJ
- Subjects
- Adult, Anemia, Sickle Cell complications, Eye Diseases etiology, Female, Fluorescein Angiography, Fundus Oculi, Hemorrhage etiology, Humans, Male, Postoperative Complications, Retinal Diseases etiology, Sarcoidosis complications, Choroid blood supply, Laser Therapy, Lasers, Retinal Diseases surgery, Vitreous Body blood supply
- Abstract
Argon laser photocoagulation performed to destroy retinal neovascularization in two patients with proliferative sickle retinopathy and one patient with sarcoidosis was complicated by the development of choroidal neovascular tissue that extended through the photocoagulated retina into the vitreous. Attempts to obliterate the neovascular growth were successful in two cases. In the case that did not respond to repeated therapeutic procedures, the possibility of a direct communication with the long posterior ciliary artery was suggested by the presence of a chorioretinal defect in the vicinity of the photocoagulated area.
- Published
- 1975
- Full Text
- View/download PDF
19. Vitamin E in kitten oxygen-induced retinopathy. II. Blockage of vitreal neovascularization.
- Author
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Phelps DL and Rosenbaum AL
- Subjects
- Animals, Cats, Placebos, Retinal Diseases etiology, Time Factors, Collateral Circulation, Oxygen Inhalation Therapy adverse effects, Retinal Diseases prevention & control, Vitamin E therapeutic use, Vitreous Body blood supply
- Abstract
The effect of vitamin E (tocopherol) on oxygen-induced retinopathy was studied in the kitten after a quantitative scoring system was developed for their India ink injected retinal flat preparations. In 75 previously described kittens exposed to two or three days of oxygen from day 3, treatment from day 1 with vitamin E or placebo disclosed that kittens treated with vitamin E had less retinopathy. Theories of the mechanism of action of vitamin E would predict that, if given only after the oxygen exposure, vitamin E should be ineffective. This was tested in 37 kittens with placebo or drug begun only after withdrawal from oxygen. Unexpectedly, significantly less intravitreal neovascularization was found in kittens treated with vitamin E after oxygen exposure.
- Published
- 1979
- Full Text
- View/download PDF
20. [No disorder of arachidonic acid-induced thrombocyte aggregation in familial exudative vitreoretinopathy].
- Author
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Bopp S, Wagner T, and Laqua H
- Subjects
- Adult, Arachidonic Acid, Blood Coagulation Tests, Child, Chromosome Disorders, Female, Humans, Pedigree, Retinal Diseases blood, Arachidonic Acids, Chromosome Aberrations genetics, Genes, Dominant, Platelet Aggregation drug effects, Retinal Diseases genetics, Vitreous Body blood supply
- Abstract
Six patients, members of a family with familial exudative vitreoretinopathy (FEVR), were studied to verify whether the disease was associated with a suspected platelet aggregation defect. No hemostaseologic defect was found in either the affected or healthy members of the family; in particular, there were no grounds for suspecting any disturbance of arachidonic acid-induced platelet aggregation.
- Published
- 1989
- Full Text
- View/download PDF
21. Familial exudative vitreoretinopathy.
- Author
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Laqua H
- Subjects
- Adolescent, Adult, Child, Exudates and Transudates, Eye Diseases genetics, Female, Fluorescein Angiography, Genes, Dominant, Humans, Male, Retinal Vessels pathology, Retinal Diseases genetics, Vitreous Body blood supply, Vitreous Body pathology
- Abstract
A pedigree of familial exudative vitreoretinopathy is presented; 12 out of 37 family members examined were affected and the inheritance pattern was compatible with an autosomal dominant disease. Clinical findings and fluorescein angiographic studies of patients with the early stages of the disease support the concept that familial exudative vitreoretinopathy is a disease primarily of the small peripheral vessels leading to peripheral fibro-vascular mass lesions.
- Published
- 1980
- Full Text
- View/download PDF
22. [Maculopathy caused by aberrant vascular adhesion of the hyaloid system].
- Author
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Cordier J and Raspiller A
- Subjects
- Child, Female, Fluorescein Angiography, Humans, Vitreous Body embryology, Macula Lutea, Retinal Diseases etiology, Vitreous Body blood supply
- Published
- 1972
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