Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A critical review of the literature of retrolental fibroplasia indicates that the cause of this disease is not yet known. Oxygen is certainly a critical factor but it is still not possible to make precise recommendations as to the amount or the duration of therapy that is safe. We have overemphasized the role of oxygen in the past, and as a result of this the false impression has been created that RLF is a disease that can be prevented. This gross oversimplification of a complex disease with multiple causes has resulted in many unjustified malpractice claims. A study of the present epidemic indicates that excessive oxygen administration probably plays a minor role, in contrast to the first epidemic in which prolonged oxygen administration was clearly a major factor. A reasonable working hypothesis is that the developing retina is highly sensitive to any disturbance in its oxygen supply, either hyperoxemic or hypoxemic. The retinal circulation is subject to the same wide fluctuations as the cerebral circulation in newborn infants. The very low-birth-weight, sick premature infant suffers from a number of conditions, many of which can seriously disturb the retinal circulation, resulting in hypoperfusion and ischemia. These factors (immaturity, hyperoxia, hypoxia, blood transfusions, intraventricular hemorrhage, apnea, infection, hypercarbia, hypocarbia, patent ductus arteriosus, prostaglandin synthetase inhibitors, vitamin E deficiency, lactic acidosis, prenatal complications, genetic factors) may all be present in an infant. They may interact to produce various degrees of retinal damage. Nearly all of these factors cannot be prevented or controlled by our present methods of care. Unfortunately, this means that RLF is an extremely difficult disease to prevent, treat, or investigate. A disease of this complexity with multiple causes will require very large numbers of infants in any controlled study of a therapy. Retrolental fibroplasia should not be considered an avoidable iatrogenic disease in very low-birth-weight infants. Its cause in these infants is not known.
 ...
PMID:A reexamination of the role of oxygen in retrolental fibroplasia. 641 99

Hypoxic brain damage and retrolental fibroplasia caused by hyperoxia can be prevented only by monitoring arterial pO2 during oxygen therapy of the newborn. The accuracy of continuous transcutaneous measurement of arterial pO2 is questionable during unstable phases of adaptation to extrauterine life, and measurement of arterial pO2 with the help of an umbilical arterial catheter (or intraarterial pO2 electrode) may therefore by mandatory. Transcutaneous continuous monitoring of paCO2 appears to afford excellent results and will soon be an indispensable adjuvant for the therapy of newborns with respiratory problems. Since the expense of monitoring is high, oxygen therapy and management of respiratory insufficiency in the newborns concerned should be transferred to centers for neonatal intensive care.
 ...
PMID:[Continuous monitoring of blood gases in newborn infants]. 681 Apr 58

A 2,948-g full-term male infant, the product of an uncomplicated pregnancy, developed fundus changes consistent with retrolental fibroplasia in the absence of supplemental oxygen therapy. He had no associated illnesses or congenital anomalies, and had not received exchange transfusions. There was no family history of ocular disease. Changes similar to those of retrolental fibroplasia do occasionally occur in fullterm infants who have had no supplemental oxygen therapy. A relative hyperoxia caused by the increase in arterial oxygen saturation occurring at birth is one possible explanation for these events. This rise, plus susceptibility factors apart from prematurity, may account for these unusual cases. Additionally, these cases may represent sporadic examples of familial exudative vitreoretinopathy.
 ...
PMID:Peripheral proliferative retinopathy without oxygen therapy in a full-term infant. 689 16

The incidence of retrolental fibroplasia (RLF, retinopathy of prematurity) is increasing, as more premature infants of lower birth weight are surviving. Currently, about 17% of premature neonates at risk will develop this condition, although in 85% of these cases it will undergo spontaneous resolution. This paper reviews our current knowledge and management of RLF, and aims to remind us that sophisticated monitoring techniques have not eliminated the problems of hyperoxia.
 ...
PMID:Retrolental fibroplasia today. 701 57

Aspirin administration, at a dosage producing plasma levels within the human therapeutic range, caused marked inhibition of production of both vascular prostacyclin (a vasodilator) and platelet thromboxane (a vasoconstrictor) in beagle puppies. In addition, aspirin-treated, oxygen-exposed puppies developed retinopathy of significantly greater severity than their unmedicated, oxygen-exposed littermates. Direct ophthalmoscopic observations indicated that whereas sustained oxygen breathing produced retinal vasoconstriction in unmedicated puppies, retinal vessels of aspirin-treated littermates became more dilated or remained unchanged. It is postulated that retinal vasoconstriction may be a normal physiologic mechanism to protect the immature retina from damaging effects of high blood oxygen levels; i.e., it may be a protective rather than a pathologic process in response to hyperoxia. Many vascular anomalies which characterize the human disease were present in the retinas of the puppies. Several of the most severely affected puppies treated with aspirin even displayed grade III cicatricial retinopathy (falciform retinal fold). Thus, a major criticism of the retrolental fibroplasia animal model has been addressed by producing cicatricial retrolental fibroplasia in puppies, and the confidence with which results from experimental animal studies might be extrapolated to the clinical situation is thereby strengthened.
 ...
PMID:Retrolental fibroplasia: evidence for a role of the prostaglandin cascade in the pathogenesis of oxygen-induced retinopathy in the newborn beagle. 702 56

D-Penicillamine, previously suspected to have a beneficial effect on the occurrence of severe retrolental fibroplasia among very low birth weight infants, was tested to determine the extent to which this drug modifies acute radiosensitivity on 3- to 4-day-old mice in comparison with adult animals. It was found that the radioprotective effect of penicillamine, given in doses of 3,000 mg/kg i.p. 60 min before whole-body exposure to 6-10 Gy of 60Co gamma rays, was greater in 3- to 4-day-old mice than in adult animals. These data seem to be compatible with the view that D-penicillamine, by virtue of its antioxidant action, may reduce the toxic effects associated with exposure of the newborn infant to hyperoxia, specifically retrolental fibroplasia and bronchopulmonary dysplasia.
 ...
PMID:Age-related difference in radioprotective effect of D-penicillamine. 715 43

Retinopathy of prematurity (ROP) is initiated by hyperoxia-induced obliteration of newly formed blood vessels in the retina of the premature newborn. We propose that vessel regression is a consequence of hyperoxia-induced withdrawal of a critical vascular survival factor. We show that regression of retinal capillaries in neonatal rats exposed to high oxygen, is preceded by a shut-off of vascular endothelial growth factor (VEGF) production by nearby neuroglial cells. Vessel regression occurs via selective apoptosis of endothelial cells. Intraocular injection of VEGF at the onset of experimental hyperoxia prevents apoptotic death of endothelial cells and rescues the retinal vasculature. These findings provide evidence for a specific angiogenic factor acting as a vascular survival factor in vivo. The system also provides a paradigm for vascular remodelling as an adaptive response to an increase in oxygen tension and suggests a novel approach to prevention of ROP.
 ...
PMID:Vascular endothelial growth factor acts as a survival factor for newly formed retinal vessels and has implications for retinopathy of prematurity. 748 57

Retinopathy of prematurity (ROP) usually occurs after a prolonged exposure to normobaric hyperoxia in newborn mammals and infants. We hypothesized that experimental ROP also could develop after acute exposures to hyperbaric oxygenation (HBO), providing that a severe and maintained retinal vasoconstriction occurred during HBO exposure. Five- to seven-day-old, Long Evans Sprague-Dawley rats were exposed for 5 h either to 5 atm abs oxygen or to 5 atm abs O2 with 190 mmHg inspired PCO2 (hypercapnia). Control rats breathed air at atmospheric pressure. Two months after exposures, rats were anesthetized, perfused intraventricularly with India ink, and retinal images were obtained. Retinal vascular density (RVD) in each image was calculated as the number of pixels in the retinal vessel area divided by the total number of pixels in the image (retinal tissue and vessels). The RVD was significantly increased from 0.0112 +/- 0.004 in the air-exposed controls to 0.0417 +/- 0.029 in the HBO-exposed rats (mean +/- SD; n = 4 in each group). HBO with hypercapnia produced a nonsignificant increase in RVD (0.0255 +/- 0.007; n = 4), reducing the HBO-induced increase in RVD by 39%. These results are consistent with the hypothesis that a sustained HBO-induced retinal vasoconstriction in newborn rats, followed by a hypoxic-ischemic injury, might result in vascular proliferation, thereby initiating ROP development on return to air. Hypercapnia does not completely prevent HBO-induced retinal vasoproliferation, probably because possible vasodilation, induced by hypercapnia, can greatly elevate retinal tissue PO2 and promote oxidative damage.
 ...
PMID:Experimental retinopathy by hyperbaric oxygenation. 774 8

This review deals with retinopathy of prematurity (ROP), a disease characterized by retinovitreal neovascularization, eventually retinal detachment and blindness. Due to the increasing number of extremely premature newborns, it is becoming more frequent. ROP of all stages occurs in 25-35% of surviving premature newborns of gestational age up to approximately 35 weeks. Stages 3 or more occur in 5-10%, blindness in 3-5% of very immature babies. The incidence is inversely related to gestational age. Classification is internationally unified (ICROP) and describes 5 stages. Its pathogenesis has not yet been clarified. More or less proven risk factors are retinovascular immaturity, hyperoxia and possibly circulatory and respiratory instability. Prophylaxis consists in avoiding hyperoxia, and probably also in keeping the extremely premature newborn stable. Ophthalmologic examinations must be performed by ophthalmologists experienced in this field or under their direct responsibility and must be standardized. Treatment of ROP can be carried out at a certain stage by coagulation therapy.
 ...
PMID:Retinopathy of prematurity. 779 Jun 13

Hyperoxia is a risk factor for retinopathy of prematurity (ROP), a blinding disease in infants. However, ROP develops in human infants without raised arterial oxygen levels, such as in cyanotic congenital heart disease. In these infants raised pCO2 may be a risk factor. We investigated the effect of inspired CO2 on oxygen induced retinopathy in the rat. 56 newborn Sprague-Dawley rats were exposed to high cyclical O2 for seven days. In a control group, 27 rats were exposed to negligible CO2 by the use of soda lime. In the high CO2 group, 29 rats were exposed to elevated CO2 by omitting soda lime from their chambers. Rats in both groups had a recovery period of three days in room air following cyclical O2 exposure. On the eleventh day all rats were sacrificed after intracardiac injections of fluorescein under deep anesthesia and the retinae were dissected and flat mounted for fluorescent microscopy. The ratio of vascularized:total retinal area was calculated using computer assisted image analysis. In the high CO2 group 62% +/- 7% SD of the retina was vascularized vs. 81% +/- 7% in low CO2 group (p < 0.001). Elevated inspired CO2 results in pronounced retardation of retinal vascular development in neonatal rats exposed to fluctuating raised oxygen.
 ...
PMID:The effect of raised inspired carbon dioxide on developing rat retinal vasculature exposed to elevated oxygen. 784 26


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>