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

During sleep, of ventilated newborns and young infants, spontaneous respiratory movements may occur, unrelated to the ventilation impulsions. The respiratory pattern is then classified as "active". On the contrary, the respiratory pattern is classified as "passive", when all respiratory movements are related to the ventilation insufflation. The factors which influence the dependence on the ventilator are studied in a group of 20 newborn and young infants. Prematurity, some biological data such as hyperoxia, hypocapnia, seem to favor this dependence. A rapid rate of ventilation (superior to 30/minute) is rarely related to an active respiration; a slow rate of ventilation seems favor this respiratory pattern. It is clear that adaptation to artificial ventilation is better during quiet sleep than during active sleep. Some physiopathological considerations are developed.
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PMID:[Assisted ventilation of newborn infants during sleep. Study of factors modifying adaptation to ventilation]. 52 40

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

We have previously shown that mRNA for caeruloplasmin, the serum copper-binding protein, is not expressed in guinea-pig liver prior to birth and expression increases rapidly following parturition. To further study the regulation of caeruloplasmin in neonatal animals we have used 3-day preterm guinea pigs, delivered by caesarean section, to investigate mRNA expression in liver and lung. Within 12 h of premature birth, hepatic caeruloplasmin mRNA levels are significantly increased and remain elevated by 72 h. This induction of expression is accompanied by an increase in circulating levels of holoprotein. Even greater induction of caeruloplasmin mRNA was observed in premature animals maintained in 95% oxygen for 72 h, confirming an acute-phase response in prematurity. Studies of lung RNA showed that caeruloplasmin mRNA is expressed throughout development, with highest levels observed in adult lung. In the premature animals levels were significantly elevated 12 h after delivery, but then fell by 72 h to below those seen in normal term lung. Hyperoxia did not influence the pulmonary mRNA levels.
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PMID:Induction of hepatic and pulmonary caeruloplasmin gene expression in developing guinea pigs following premature delivery. 162 60

Microvascular cells are most vulnerable to direct oxygen damage. Using an in vitro model system we have investigated the effect of elevated oxygen on the proliferation, morphology, and integrity of microvascular endothelial cells (EC) and pericytes. Cultivation of these cells at oxygen concentrations of 40% for 1 wk resulted in the inhibition of EC proliferation but had no effect on the growth of the pericytes. Similarly, hyperoxia induced a dramatic change in the shape of the EC, increasing their spread area by close to six-fold. Under the same conditions, the spread area of the pericytes was unaffected. To understand the effect of the hyperoxic treatment on the cells, the integrity of various membrane systems was assessed. 51Chromium release was used to monitor plasma membrane integrity. There was no difference in chromium release by EC and pericytes over the 7 d of growth under normoxic and hyperoxic conditions. Mitochondrial integrity was examined by staining the cells with Rhodamine 123, which is selectively accumulated by the mitochondria. The staining pattern of the mitochondria of both EC and pericytes was altered by growth in the elevated oxygen. Finally, the lysosomes were visualized using acridine orange. The acridine orange staining pattern revealed enlarged and perinuclear lysosomes in the EC but no change in the pericyte lysosomal staining pattern. Thus, the cells of the microvasculature seem to be differentially affected by hyperoxia, a fact that may be significant in the etiology of reperfusion injury, ischemic disease, and pathologies associated with prematurity.
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PMID:Effects of hyperoxia on microvascular cells in vitro. 243 58

Yellow staining of central nervous system (CNS) nuclei occurs in the brains of some neonates, despite low levels of serum bilirubin. Two conditions appear to be important in the evolution of this form of kernicterus: prematurity and asphyxia. In a seven year retrospective study of a large neonatal autopsy population, 102 cases had kernicterus as indicated by selective macroscopic yellow staining and microscopic damage within specific CNS nuclei. Neuropathological study disclosed minor variations and numerous similarities in the manifestations of kernicterus in the asphyctic premature neonate with low levels of serum bilirubin, as compared to kernicterus in the full-term neonate with high levels of serum bilirubin. Acidosis, hypoxia, hyperoxia, hypothermia and sepsis have been considered significant risk factors, but recent comparative clinical studies have not defined predictive indices. Analysis of this disorder is difficult because of the concurrence of other complications of asphyxia and its pathological correlates in premature infants. Diagnostic difficulties are also compounded by variations in the definitions of kernicterus as used by different investigators.
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PMID:The neuropathology of kernicterus in the premature neonate: diagnostic problems. 669 27

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.
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PMID:Peripheral proliferative retinopathy without oxygen therapy in a full-term infant. 689 16

Dietary or chemical depletion of pulmonary glutathione in adult rats and mice, has been demonstrated to exacerbate the toxic effects of high oxygen concentrations. The present paper has examined this phenomenon in a guinea-pig model of prematurity, using the electrophilic agent diethylmaleic acid (DEM) to provide a transient (up to 12 h) pulmonary glutathione depletion. Full-term and 3-days preterm guinea-pig pups were studied to assess the possible role for glutathione deficiency as a mechanism mediating the increased susceptibility of the immature lung to oxygen free-radical damage. The administration of DEM to guinea-pig neonates depleted lung glutathione by 90% (term) or 68% (preterm) over 2 h. On exposure of pups to 95% oxygen for 48 h, DEM increased the incidence of oxygen-related death to 31% in term pups and 100% in preterm pups. Term pups exposed to hyperoxia and treated with DEM showed evidence of pulmonary injury, indicated by an influx of neutrophils into the lung airspaces, and elevated microvascular permeability. Control pups exposed to 95% oxygen were found to have uninjured lungs after 48 h. We conclude that glutathione is an essential component of the pulmonary antioxidant array in neonates. Glutathione may be of particular importance in the early phase of oxygen exposure. The deficiency of lung glutathione observed in preterm animals may account for their increased susceptibility to oxygen-induced pulmonary injury.
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PMID:Depletion of pulmonary glutathione using diethylmaleic acid accelerates the development of oxygen-induced lung injury in term and preterm guinea-pig neonates. 802 13

In recent years increasing experimental and clinical data have provided compelling evidence for the involvement of oxygen free radicals in the 3 main disorders of prematurity--chronic lung disease, retinopathy of prematurity and intraventricular haemorrhage. Infants born prior to 30 weeks gestation or weighing less than 1500 g at birth appear to be most at risk. They are very underdeveloped and as a consequence of the immaturity of their lungs often require intense respiratory support, including the provision of supplemental oxygen. The theoretical basis for free radical involvement in these disorders is that oxygen centred radicals and related reactive oxygen metabolites are formed too rapidly to be detoxified by the antioxidant defence mechanisms in specific tissues. In the case of chronic lung disease, the evidence currently favours excess oxygen (hyperoxia) as the cause of the greater oxygen free radical production, whereas in retinopathy of prematurity and intraventricular haemorrhage, it is proposed that low oxygen tensions (hypoxia) followed by periods of reoxygenation is the more likely stimulus for excess radical formation.
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PMID:Free radical disorders of preterm infants. 822 Oct 31

The therapeutic efficacy of N-acetylcysteine (NAC) in the management of hyperoxia-induced lung injury was assessed using the preterm guinea pig model of prematurity. Preterm guinea pig pups were delivered by Caesarean section 3 days preterm, and exposed to either 21 or 95% oxygen for 72 hr. NAC (200 mg/kg body weight) or saline was injected twice daily. Bronchoalveolar lavage fluid (BALF) from hyperoxia-exposed pups contained significantly higher protein concentrations and an increased number of neutrophils. NAC partly ameliorated lung injury, preventing the increase in BALF protein concentration, which is generally associated with oedema. There was no effect on the movement of neutrophils into the lung airspaces in response to oxygen. Treatment with NAC had no effect on lung or liver glutathione (reduced) (GSH) concentrations either after 2 hr post-administration, or over the full 72 hr experimental period. An apparent resistance of the lung to increased synthesis or uptake of GSH was demonstrated by the lack of effect of direct administration of GSH, its isopropyl ester or 2-oxo-4-thiazolidine carboxylic acid. Oxygen exposure alone (95%) increased lung concentrations by 60-70%. It would, therefore, appear from this data that NAC may have potential as a future component of antioxidant therapy, although its effects are not mediated through increased GSH levels.
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PMID:N-acetylcysteine ameliorates hyperoxic lung injury in the preterm guinea pig. 845 59


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