Experimental Retinal Branch Vein Occlusion
About: This article is published in American Journal of Ophthalmology.The article was published on 1970-05-01. It has received 103 citations till now.
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TL;DR: Correct control of the multiple pathways, such as retinal blood flow, tissue oxygenation and metabolic substrate support, aiming at restoring retinal cell metabolic interactions, may be effective in preventing damage occurring during the evolution of ischemic microangiopathies.
511 citations
Cites background from "Experimental Retinal Branch Vein Oc..."
...Hypoxia-induced damage of the neuronal cells in the inner retina has been confirmed by histology (Kohner et al., 1970; Hockley et al., 1979; Pournaras et al., 1990b)....
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TL;DR: Occlusions of nine branch retinal veins in eight eyes of seven patients were studied histopathologically by serial sections through the affected areas, and no definite thrombus was observed in any of them.
Abstract: • Occlusions of nine branch retinal veins in eight eyes of seven patients were studied histopathologically by serial sections through the affected areas. Intravitreal neovascularization from the disc, retina, or both was noted in four eyes. Two additional eyes had intraretinal neovascularization (intraretinal microvascular abnormalities). Cystoid macular edema was present in five eyes. A fresh or recanalized thrombus was noted at the site of vein occlusion in all eyes. Inner ischemic atrophy of the retina was found distal to the area of occlusion in six of the nine affected quadrants of the eight eyes. Although the corresponding branch retinal arteries showed varying degrees of sclerosis (severe, three eyes; moderate, five eyes; and minimal, one eye), no definite thrombus was observed in any of them.
209 citations
TL;DR: The treatment of branch retinal vein occlusion may possibly benefit from a refined angiographic analysis of the process of collateral formation and new treatment methods aimed at accelerating the processof collateral maturation.
165 citations
157 citations
TL;DR: The authors emphasize the need for well-controlled randomized studies to evaluate the natural history of branch vein occlusion and the efficacy of photocoagulation in its treatment.
156 citations
References
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TL;DR: Noteworthy has been the predominant localization of the diabetic microaneurysms in the central and paracentral regions, their random distribution, and their association with punctate hemorrhages and "exudates" in the deep retina.
Abstract: It is generally held that microaneurysms constitute the characteristic lesion of diabetic retinopathy. First observed by MacKenzie and Nettleship in 1879, 1 the microaneurysms were rediscovered by Ballantyne and Loewenstein in 1943 2 and have been described by numerous clinicians and pathologists since that time. Noteworthy has been the predominant localization of the diabetic microaneurysms in the central and paracentral regions, their random distribution, and their association with punctate hemorrhages and "exudates" in the deep retina. It has also been assumed that the microaneurysms and other evidence of angiopathy in diabetic retinas have a bearing on the glomerular changes in diabetic nephropathy 3-5 and that a clarification of the one might yield useful information for the other. As must be evident from the many reviews which have appeared in recent years, 6-12 the pathogenesis of retinal microaneurysms has been a subject of wide speculation based on some firm evidence but
715 citations
TL;DR: Three of the most important manifestations of diabetic retinopathy will be discussed, namely endothelial proliferation, capillary microaneurysms, and capillary closure.
Abstract: ONLY 10 years ago laboratory research on the problem of diabetic retinopathy was confined to a few investigators working in isolated ophthalmological centres, but to-day it is attracting widespread attention from many different quarters and the literature is alive with new observations and new theories. It is therefore timely to consider to what extent the various pathological features of the disease may be specific for diabetes or simply fundamental reactions to non-specific injury. I should like to consider some recent findings from my own and other laboratories which throw further light on normal and abnormal reactions of retinal capillaries, and to discuss their possible relation to the pathological picture of diabetic retinopathy and to some of the theories of pathogenesis which have been advanced. Three of its most important manifestations will be discussed, namely endothelial proliferation, capillary microaneurysms, and capillary closure. The question of venous dilatation is a clinical one, and there is still not complete agreement that it is an early sign of diabetic retinopathy, and I shall not therefore deal with it as a pathological entity. Everyone would surely agree that the exudates are of only secondary importance. Before discussing these three pathological manifestations, a few comments will be made on our technical methods and upon the normal retinal capillaries.
236 citations
TL;DR: The granule extract can digest vascular basement membrane in vitro at neutral pH and basement membranes of blood vessels damaged in vivo by the leukocyte fraction are found to be attenuated when examined by electron microscopy.
Abstract: Frozen and thawed granules of human, peripheral-blood leukocytes rapidly produce hemorrhage when injected into animal tissues. The effect is blocked by inhibitors of proteolysis. The granule extract can digest vascular basement membrane in vitro at neutral pH. In addition, basement membranes of blood vessels damaged in vivo by the leukocyte fraction are found to be attenuated when examined by electron microscopy. The proteases of human leukocyte granules differ in several important respects from known lysosomal cathepsins and trypsin-like esterases. Polymorphonuclear neutrophils are a major source of the neutral proteases present in circulating white cells, and release these enzymes during phagocytosis of immune complexes.
198 citations
TL;DR: The clinical findings in cases of so-called central retinal venous occlusion have suggested from time to time the possible involvement of the retinal arteries as well as the veins, and a close association between the two.
Abstract: A CONSIDERATON of the occlusion of the central retinal vein cannot be regarded as a new thing because a tremendous amount of literature exists on the subject. In spite ofthis, there are many lacunae in our knowledge, so that the existing information cannot explain all the various aspects of the clinico-pathological picture of central retinal vein occlusion. Any additional data based on experimental observations may help to resolve the numerous speculations and discussions that have continued until now. The clinical findings in cases of so-called central retinal venous occlusion have suggested from time to time the possible involvement of the retinal arteries as well as the veins, and a close association between the two. This has been particularly so because of the following observations: (1) Frequent association of central retinal vein occlusion with old age, arteriosclerotic changes, and arterial hypertension. (2) The occurrence of a sector defect in the field of vision in cases of branch occlusion similar to that of an arterial branch occlusion. (3) A very high incidence of permanent blindness in cases of clinical retinal venous occlusion (Cassady (1953) saw it in 80 per cent.). (4) The histopathological examination in cases of obstruction of the central retinal vein shows atrophy of the inner layers of the retina up to the inner nuclear layer, though the visual cells are not affected (Elwyn, 1946), a picture similar to that of arterial occlusion. Recently, while investigating the pathogenesis of oedema of the optic disc (papilloedema) (Hayreh, 1964), some interesting observations on this aspect of central retinal venous occlusion were recorded on direct blockage of the central retinal vessels in Rhesus monkeys. These have been considered worth reporting in detail.
125 citations
TL;DR: Methods and findings in relation to inner and outer layers of Ganglion cell layer, Haemorrhages, and Retinal Macrophages are presented.
Abstract: Methods .. . . . .326 (ii) Ganglion cell layer . ..332 (iii) Inner plexiform layer . ..332 Findings .. . . . .326 (iv) Inner nuclear layer . ..332 (v) Outer plexiform layer . .. 332 Light Microscopy . .. . ..326 Fourteen-day Specimen .. . .332 One-hour specimen .. . .326 (i) Nerve fibre layer. . .. 332 Five-hour specimen .. . .327 (ii) Ganglion cell layer . ..333 Twenty-four-hour specimen . ..327 (iii) Inner plexiform layer . .. 333 Three-day specimen .. . .327 (iv) Inner nuclear layer . ..333 Seven-day specimen .. . .327 (v) Outer plexiform layer . ..333 Fourteen-day specimen .. . .327 Twenty-five-day Specimen . ..333 Twenty-five-day specimen . ..328 (i) Inner layers .. . .333 Haemorrhages . .. . ..328 (ii) Outer plexiform layer . ..334 Retinal Macrophages .. . .334
87 citations