[CLINICAL AND EXPERIMENTAL STUDY OF AMITRITRIPTYLINE ON RETINAL VASCULARIZATION IN ATHEROMATOUS SUBJECTS].
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Amitriptyline↗
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Results for “Retinal Neovascularization”
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A macular hole in a female adult with bilateral coats disease.
PURPOSE: To report a case of a macular hole in a female adult with bilateral Coats disease. METHODS: The fundus photograph, fundus fluorescein angiography (FFA) and indocyanine green angiography (ICGA) were performed in two eyes, and observed theirs characters. RESULTS: Fundus photograph showed massive yellowish-white exudation in the temporal midperiphery of both eyes, but the degree was slighter in the right eye. There was 1/3 DD macular hole in left eye. FFA revealed general dilatation of capillaries, multiple aneurysms, and tortuous and closure of vessels in superotemporal midperiphery in both eyes, but the degree was slighter in the right eye. There was a one-third DD round transmitted fluorescence according the macula hole. ICGA revealed that hyperfluorescence of aneurysms in superotemporal midperiphery, the images of aneurysms were more clearly than in FFA. There was a 2/3 DD hypoflurescence of macula in the late phase of angiography. CONCLUSIONS: FFA and ICGA have respective advantage in revealing vascular abnormalities of Coats disease. Maybe there was some relationship between the abnormalities of retinal vascular and hypoperfusion of choroidial vascular in macula in this case.
Adult↗
[The role of vascular endothelial growth factor (VEGF)].
The authors present the role of VEGF in microaneurysm formation, blood-retinal barrier breakdown, development of capillary nonperfusion and retinal neovascularization in pathogenesis of diabetic retinopathy. Inhibitors of VEGF in treatment of diabetic retinopathy are presented.
Aneurysm↗
Eales disease with internuclear ophthalmoplegia.
Eales disease is an idiopathic type of retinal perivasculitis characterized by recurrent retinal and vitreous hemorrhages. Neurologic involvement is rare. We report the case of a patient with Eales disease who had internuclear ophthalmoplegia thought to be a neurologic manifestation of this disease.
Adult↗
Ophthaproblem. Retinal arteriovenous malformations (type 2).
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Aged↗
Vascular changes and their mechanisms in the feline model of retinopathy of prematurity.
This study documents changes to retinal vasculature during the feline form of retinopathy of prematurity (ROP). The authors describe the closure and obliteration of retinal vessels during exposure to high oxygen, the pattern and tempo of growth of proliferative vasculature, which, after the return of the animal to room air, extends from the optic disc in a spectacular "rosette" pattern, the formation of preretinal vascular growths, and an initial lack of barrier properties in the new vessels. Finally, the response of the vasculature to the relief of hypoxia is reported, including the gradual establishment of barrier properties in the intraretinal vessels, the partial normalization of the proliferative vessels, and the abnormalities that persist. It is suggested that the vascular changes occur in successive stages: closure and obliteration during hyperoxia, vasoproliferation induced by hypoxia, and normalization after the relief of hypoxia with distinct cellular mechanisms and stimuli. It is argued that the same stages can be seen in the human form of ROP; two possible stimuli for the fibroplasia that damages the retina in human ROP are discussed.
Animals↗
Degeneration of astrocytes in feline retinopathy of prematurity causes failure of the blood-retinal barrier.
This study addresses the role of astrocytes in the genesis of retinopathy of prematurity, examined in the feline model of this condition. Evidence is presented that the hypoxia of retinopathy of prematurity, in addition to inducing vasoproliferation, damages the retina directly. Retinal neurons survive the hypoxia, but the astrocytes, which are involved in the formation of the glia limitans of the retinal vessels, degenerate. Astrocytes subsequently recolonize the retina after a delay that matches the period of leakiness of the proliferative vasculature (described in the companion article). Given the evidence from other studies that the barrier properties of vessels are induced by their glia limitans, the authors suggest that the initial lack of barrier properties in the new vasculature is caused by the degeneration of astrocytes and that the subsequent formation of those properties is induced by the astrocytes that recolonize the retina some days later. The observation that astrocytes are more sensitive to hypoxia than neurons, at least in developing tissue, was unexpected. The literature reporting on the damage caused to central nervous tissue by hypoxia is consistent in assessing neurons as more sensitive and glial changes as a reaction to neuronal damage. The sensitivity of astrocytes found in this study and earlier in vitro research suggests that degenerated astrocytes can be replaced and their structural and functional relationships reestablished.
Animals↗
The renin-angiotensin system and diabetic retinopathy.
The importance of the renin-angiotensin system in the eye has not been clearly established, nor is it known whether it is of importance in the evolution of diabetic retinopathy. Circulating renin is produced in the kidney and other tissues; its main importance is in the control of blood pressure. Elevated levels have been found in diabetic patients with microvascular complications. There is also some suggestion that the prorenin content is elevated in diabetics and that this is an indicator of the development of microvascular complications in the next few years. Angiotensin-converting enzyme (ACE) inhibitors have been found to reduce the leakage in early diabetic retinopathy, but it is possible that this was only due to a reduction of blood pressure. Angiotensin II was found to induce neovascularisation in corneal pocket experiments, and the replication of aortic endothelial cells has been reported. We were unable to find any increased replication of retinal endothelial cells treated with angiotensin II. It is possible that the main function of the renin-angiotensin system in the eye is the regulation of local blood flow.
Angiotensin-Converting Enzyme Inhibitors↗
[Morphopathological study in age related macular degeneration].
UNLABELLED: The aim of this paper is to study the morphopathological changes manifested in age-related macular degeneration. MATERIAL AND METHOD: The researched histopathological material consisted in two eye balls enucleated because of irreversible eye diseases from aged persons suffering from age-related macular degeneration. The method applied for processing the material was inclusion in paraffin, followed by usual coloration with hematoxylin-eosin. RESULTS AND CONCLUSIONS: The established changes (hard drusen, soft drusen, calcified drusen, changes of Bruch's membrane, subretinal neovascularization, serous retinal pigment epithelial detachment, disciform degeneration) prove the importance of Bruch's membrane in the pathogenesis of age-related macular degeneration.
Aged↗
Does hypertension play a role in diabetic retinopathy?
Diabetic retinopathy is a common complication of diabetes. It represents one of the frequent causes of visual disability among diabetic subjects during the period of active life. The risk factors for diabetic retinopathy are poor glycemic control, hypertension, duration of diabetes, hyperlipidemia and proteinuria. It has been observed that prevalence of hypertension is higher in diabetic subjects than in the general population and as it also plays a major role in the progression of diabetic retinopathy, so tight control of hypertension is mandatory. The possible mechanisms by which hypertension affects diabetic retinopathy are haemodynamic (impaired autoregulation and hyperperfusion) and secondly through VEGF (Vascular Endothelial Growth Factor), as it has been observed that hypertension independent of hyperglycaemia upregulates the VEGF expression in retinal endothelial cells and ocular fluids. The level of control of blood pressure are debatable but nearer the blood pressure to the normal levels, better the chances of preventing the onset and progression of diabetic retinopathy. The lowering of blood pressure to a normal range is more important than the type of antihypertensive medication used. Diabetic retinopathy is one of the important causes of visual disability in diabetic subjects during the period of active life. It is characterized by gradually progressive alterations in the retinal microvasculature, leading to increased vasopermeability, areas of retinal occlusion and retinal neovascularization. The complications associated with increased vasopermeability and uncontrolled neovascularization can result in severe and permanent visual loss.
Comorbidity↗
[Critical evaluation of the treatment of diabetic retinopathy based on personal experience].
The authors present the results of analysis of the treatment of 184 patients (360 eyes) with diabetic retinopathy; it comprises as well the out-patients as the in-patients divided into 4 groups in dependence on the changes and the treatment applied (laser focused photocoagulation, panretinal photocoagulation, cryopexy) the majority of patients reported to the hospital with an advanced proliferative diabetic retinopathy and this allowed only the performance of a panretinal photocoagulation and in a part of cases only cryopexy. The attention is called to the necessity of an early detection of pathological changes and of an early treatment.
Adult↗
[Peripheral photocoagulation of the retina in the treatment of early forms of diabetic retinopathy].
The authors present the results of a 5 years long observation of patients with an early form of diabetic retinopathy in whom one performed a photocoagulation of the retinal periphery. They observed the behavior of the visual function and the changes in the anterior chamber angle.
Adult↗
Proceedings of the Third International Symposium on Retinopathy of Prematurity: an update on ROP from the lab to the nursery (November 2003, Anaheim, California).
The Third International Symposium on Retinopathy of Prematurity (ROP) was convened with the aim of cross fertilizing the horizons of basic and clinical scientists with an interest in the pathogenesis and management of infants with ROP. Ten speakers in the clinical sciences and ten speakers in the basic sciences were recruited on the basis of their research to provide state of the art talks. The meeting was held November 9, 2003 immediately prior to the American Academy of Ophthalmology meeting; scholarships were provided for outreach to developing countries and young investigators. This review contain the summaries of the 20 platform presentations prepared by the authors and the abstracts of presented posters. Each author was asked to encapsulate the current state of understanding, identify areas of controversy, and make recommendations for future research. The basic science presentations included insights into the development of the human retinal vasculature, animal models for ROP, growth factors that affect normal development and ROP, and promising new therapeutic approaches to treating ROP like VEGF targeting, inhibition of proteases, stem cells, ribozymes to silence genes, and gene therapy to deliver antiangiogenic agents. The clinical presentations included new insights into oxygen management, updates on the CRYO-ROP and ETROP studies, visual function in childhood following ROP, the neural retina in ROP, screening for ROP, management of stage 3 and 4 ROP, ROP in the third world, and the complications of ROP in adult life. The meeting resulted in a penetrating exchange between clinicians and basic scientists, which provided great insights for conference attendees. The effect of preterm delivery on the normal cross-talk of neuroretinal and retinal vascular development is a fertile ground for discovering new understanding of the processes involved both in normal development and in retinal neovascular disorders. The meeting also suggested promising potential therapeutic interventions on the horizon for ROP.
Humans↗
[Analysis of the protein pattern in physiologic and pathologic vitreous bodies by electrophoresis and immunologic identification].
The protein composition of normal and pathological human vitreous was analyzed using gradient SDS-PAGE and western blot. By electroblotting and immunodetection, the presence of ten proteins was proven in the normal vitreous. The major proteins included: albumin, transferrin, alpha-1-antitrypsin, and immunoglobulin G. For the detection of a distinct protein in the vitreous, western blot analysis seems to be an appropriate method. Using densitometric analysis of silver-stained gels, we compared the protein pattern of post-mortem vitreous, surgically obtained samples (from proliferative vitreous-retinopathy, proliferative diabetic retinopathy, and macular pucker patients), and serum. The protein composition of the pathological intraocular fluid was uniform, but different from that of normal vitreous and serum. These results suggest that a breakdown of the blood-retina barrier is the main reason for the increase of soluble proteins in the vitreous cavity under pathological conditions. The methods described allow detailed analysis of the vitreous protein pattern in intraocular proliferative disorders with a small sample volume (10 microliters).
Blood-Retinal Barrier↗
The use of perfluorodecalin in diabetic vitrectomy.
Nine patients were operated on for severe proliferative diabetic retinopathy using a perfluorocarbon liquid, purified perfluorodecalin; 7 patients were operated on for traction-rhegmatogenous retinal detachment, 2 for severe fibrovascular proliferation complicated intraoperatively by iatrogenic holes with surrounding retinal detachment. The intraoperative use of perfluorodecalin allowed flattening of the retina and endophotocoagulation to be carried out easily. Perfluorodecalin was removed at the end of the procedure, and intraocular tamponade was provided by silicone oil in 5 eyes and by a long-acting gas in 4 eyes. Anatomic success was obtained in 8/9 cases with a minimum follow-up of six months; 4 eyes had improved vision, 2 had the same vision, and 3 had decreased vision. The main advantage of intraoperative use of perfluordecalin is to allow easy flattening of the retina and effective endophotocoagulation under optimal visual conditions.
Adult↗
[Methods of examination of the angiogenetic activity of the retina].
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Allantois↗
Optociliary shunts and sickle retinopathy in a woman with sickle cell trait.
We report a case of unilateral optociliary shunt vessels and sickle cell retinopathy in a patient with sickle cell trait. Sickle cell retinopathy has rarely been reported in patients with sickle cell trait hemoglobinopathy. To our knowledge, this is the first report of the association of sickle cell trait, unilateral sickle cell retinopathy, and ipsilateral optociliary shunt vessels.
Anemia, Sickle Cell↗
Effect of changes in oxygen tension on vascular and platelet hydroxyacid metabolites. II. Hypoxia increases 15-hydroxyeicosatetraenoic acid, a proangiogenic metabolite.
Current strict O2 management may be precipitating more severe retinopathy of prematurity than would occur with a more lenient approach. Hypoxemia in an animal model has also been found to worsen retinal neovascularization. It has recently been shown that the hydroxyeicosatetraenoic acids can modulate angiogenesis. 15-Hydroxyeicosatetraenoic acid is proangiogenic, whereas 12-hydroxyeicosatetraenoic acid is an antiangiogenic metabolite. In vitro exposure of paired human neonatal vessels (n = 7) to hypoxia enhanced the production of total vascular hydroxyacids (232 +/- 36 pmol/mg of protein [experimental group] nu 168 +/- 31 pmol [control group]; P less than .01). The increase in vascular 15-hydroxyeicosatetraenoic acid under hypoxic conditions was even more significant (P less than .001). However, platelet production of 12-hydroxyeicosatetraenoic acid was not significantly affected by hypoxia. These observations suggest a possible biochemical basis for the abnormal angiogenic process that occurs during the proliferation phase of the retinopathy of prematurity. The production of local hydroxyeicosatetraenoic acids in tissues manifesting abnormal neovascularization needs to be further evaluated.
12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗