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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A refined classification of the stages of the retinopathy of prematurity (RLF) based on the experience of over 7500 examinations during the past decade is presented. We have been using the basic elements of this classification since 1972 in order to evaluate the influence of vitamin E on retrolental fibroplasia (RLF). It is our impression that it provides a more accurate clinical method of following the course of the retinopathy and a tool for assessing the factors other than prematurity and hyperoxia that may play a subtle role in the development of RLF.
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PMID:A classification of retrolental fibroplasia to evaluate vitamin E therapy. 58 96

The effects of oxygen in the immature or incompletely vascularized retina are conveniently divided into an initial vasoconstrictive and obliterative stage and a secondary vasoproliferative response that occurs after removal of the subject from an enriched oxygen environment. Vasoproliferation starts at the zone of perfused and nonperfused retina. The incompletely vascularized retina is uniquely responsive to these oxygen-induced changes. After vascularization is complete and the retinal vessels reach the ora, the susceptibility to hyperoxia disappears. The vessels in the temporal periphery of the retina have a peculiar susceptibility to the primary and secondary effects of hyperoxia on the immature retina. Ophthalmoscopic examination of the temporal periphery therefore should always be done carefully in the premature infant or in older individuals giving a history of prematurity. The indirect ophthalmoscope provides the most satisfactory instrument for examination. The incidence of retrolental fibroplasia has been greatly reduced following the incrimination of oxygen as its principal cause. Further studies are still required to determine precise blood oxygen levels that are safe for the premature retina and to discover other factors that may play a role in the pathogenesis or RLF.
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PMID:The role of oxygen in retrolental fibroplasia. 107 6

Rearing neonatal rats in hyperoxia induces the development of retinal hemorrhages and retinal dysplasia. Albino rats were placed in 80% oxygen immediately after birth and were exposed for either 5, 10, or 14 days, followed by sacrifice or exposure to normoxia for an additional 2, 4, 5, 7, 8, 10, 38, 45 or 56 days. Control rats were simultaneously raised in room air and sacrificed at the same times. All animals were enucleated and their eyes processed for light and electron microscopy. Eyecups were trimmed to facilitate cross-sectioning of the retina in the vertical meridian. No control rats showed signs of retinal hemorrhages or of dysplastic folds or rosettes. Nor did the retinas of rats killed immediately after oxygen exposure contain hemorrhages, but the incidence of retinal folds or rosettes in this group was 54%. For rats exposed to combinations of hyperoxia and brief normoxia (10 days or less), 40% suffered hemorrhages and 50% developed retinal folds or rosettes. Although hemorrhages were more prominent in rats subjected to longer periods of oxygen (73% of all rats exposed for 14 days followed by brief normoxia vs. 6% of those exposed for 5 days followed by brief normoxia), the incidence decreased with time post-exposure in room air. Hemorrhages occurred in 100% of the rats raised in oxygen for 14 days followed by 2 days in room air, and decreased to 50% by 7 days in room air and to 0% by 38 days, indicating a spontaneous resolution with time. In each case, the blood appeared to leak from the newly-forming vessels of the deep capillary net, with most of the red blood cells migrating to the subretinal space. Retinal fold or rosette formation, indicative of developmental dysplasia, occurred in a fraction of virtually all groups of exposed rats, and persisted at the longest post-exposure periods. These two manifestations of oxygen-induced retinopathy are emphasized because they lead to an abnormal separation of the retina from the epithelial layer, which may increase the likelihood of the most serious consequence of ROP--retinal detachment. In fact, all rats that endured post-exposure periods of 38 days or longer before sacrifice exhibited retinal detachment.
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PMID:Oxygen-induced retinopathy in the rat: hemorrhages and dysplasias may lead to retinal detachment. 145 26

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.
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PMID:Vascular changes and their mechanisms in the feline model of retinopathy of prematurity. 160 24

In order to overcome the scarcity of premature human ocular tissues and the enormous obstacles to direct examination of immature human ocular vasculatures, a number of animal models have been employed by investigators in order to study various aspects of ROP. A variety of factors may influence selection of the particular model used, but ultimately it is the faithfulness with which the model mimics human ROP that is most important. The validity of the models has been and remains a controversial subject, but evidence appears strong in favor of the beagle puppy model for studying physiology of the ocular vasculatures during perinatal development. Human ROP pathology usually is defined in terms of static morphological state, physiological dysfunction being considerably more difficult to assess. Most of the animal models fall short of mimicking the pathological lesions found in human eyes, especially those associated with severe, or end-stage ROP, yet they do fairly well in terms of mimicking the retinal vascular physiological changes associated with onset of the disease. Unfortunately, where the physiological aspects of ROP are concerned, focus is primarily on the effects of hyperoxia; other physiological factors as well as the potential role of the choroid are essentially ignored. This paper discusses the potential of physiological changes which occur during the perinatal period to play a role in ROP pathogenesis.
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PMID:Perinatal ocular physiology and ROP in the experimental animal model. 220 72

The neonatal rat, which has an immature retinal vasculature at the time of birth, is a potential animal model for retinopathy of prematurity since it has an established spindle cell retinal vasoformation pattern similar to that seen in the human. To determine if proliferative oxygen-induced retinopathy can be produced in the rat, 40 newborn rat pups were exposed from birth either to air for 25 days or to an 80% oxygen environment for 10 days, followed by 15 days in air. Extraretinal neovascularization was observed in 80% (16/20) of the rat pups exposed to hyperoxia (p less than 0.001) with a bilaterality of 87.5% (14/16). Mild to moderate vitreous hemorrhage was seen in only three eyes. Mesenchymal shunt or ridge formation was not demonstrated, nor was retinal detachment.
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PMID:Oxygen-induced proliferative retinopathy in the newborn rat. 235 94

Although oxygen has been known to be toxic for more than 200 years, the clinical importance of oxygen toxicity was not appreciated until an epidemic of retrolental fibroplasia occurred in the early 1950s. Oxygen at high partial pressures is toxic to the respiratory, cardiovascular, nervous, and gastrointestinal systems. Toxicity results from the formation of oxygen-free radicals. These arise within mitochondria as oxygen is reduced to water, as byproducts of prostaglandin and thromboxane synthesis, and by the xanthine oxidase catalyzed reduction of xanthine or hypoxanthine. They are also produced by activated macrophages as part of the immune response. Superoxide anion is the radical most commonly produced. It dismutes to hydrogen peroxide, which is able to diffuse through lipid membranes. Hydrogen peroxide reacts with transition metals to produce the highly reactive hydroxyl radical which can initiate chain reactions of lipid peroxidation leading to cell rupture. Oxygen radical scavengers such as superoxide dismutase and catalase protect the body against normal levels of oxygen-free radicals. Oxygen toxicity can result from either reperfusion of ischemic tissue or prolonged exposure to high concentrations of oxygen. Limiting hyperoxia to maintain arterial oxygen percent saturation (SaO2) greater than or equal to 90% is recommended.
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PMID:Oxygen toxicity: an introduction. 267 91

Ocular blood flow was studied in newborn piglets during light exposure and light combined with hyperoxia. Light caused a significant increase in ocular blood flow which returned to values not significantly different from baseline levels during superimposed hyperoxia. None of these experimental conditions changed total cerebral blood flow or cardiac output. The findings indicate that light might be a regulator of ocular blood flow. This influence of light on ocular blood flow may be of importance in the pathophysiology of retinopathy of prematurity.
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PMID:Effect of light and hyperoxia on ocular blood flow in the newborn piglet. 274 41

In the period from September 1983 until June 1986 a prospective study was carried out to determine the incidence and severity of retinopathy of prematurity in inborn infants of less than 1500 g at birth and the risk factors associated with the development of retinopathy of prematurity in infants of less than 31 weeks' gestation. One hundred and forty four infants were eligible for inclusion in the study. Altogether 140 infants of less than 1500 g birth weight were examined, 42 (30%) of whom developed retinopathy of prematurity. Fifteen of these infants had progression to advanced disease (stage III or stage IV). One hundred and seventeen of the infants were of less than 31 weeks' gestation and 34 (29%) of them developed retinopathy of prematurity. Thirty four risk factors shown previously to be associated with the development of the disease were collected prospectively and analysed using multiple logistic regression analysis to determine the independently significant variables. Three risk factors: acidosis, the number of times that the pH was less than 7.2; hyperoxia, the number of times that arterial oxygen tension was greater than 12 kPa; and gestational age were found to be independently associated with the development of retinopathy of prematurity in these infants. These findings suggest that acidosis may be an important aetiological factor in the pathogenesis of this disease.
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PMID:Clinical factors associated with retinopathy of prematurity. 338 68

Review of 50 histopathologic cases and a number of clinical cases of congenital retinal anomalies has permitted classification under the following headings: 1) Coloboma-orbital cyst--"anophthalmos" group due to aberrant closure of the embryonic fissure; 2) Retinal fold-central stalk-detachment group comprising a series that varies from simple retinal folds to total retinal detachment and anomalous stalk formation. Cases of the 13-15 trisomy syndrome constitute a special subgroup in this rubric; 3) Retrolental fibroplasia, due to hyperoxia of premature infants, is manifest by "dragged" disks and gliovascular proliferation with occasional detachment; 4) Persistent hyaloid system is occasionally associated with mild anomalies of the retina; 5) Massive gliosis of the retina is usually a hamartomatous manifestation; 6) Congenital absence of ganglion cells occurs with cerebral maldevelopment and 7) Congenital absence of the photoreceptors is the congenital form of retinitis pigmentosa.
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PMID:Congenital anomalies of the retina. 517 77


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