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

An Ohmeda Biox 3700 oximeter was evaluated during treatment of 12 patients with respiratory distress. The infants were of 27-33 weeks' gestation and between 2 days and 5 months postnatal age. Blood gases were taken from indwelling arterial catheters and were measured on an ABL 30 blood gas analyser. The study tested the accuracy of the oximeter in detecting hypoxia (PaO2 less than 55 mmHg) and hyperoxia (PaO2 greater than 80 mmHg). Results are based on 175 paired observations. Guidelines are suggested for the use of the pulse oximeter under three conditions. In a newborn infant with acute respiratory distress without direct arterial access, the limits should be set at 85% (lower) and 90% (upper). In an older infant with chronic respiratory distress, the upper limit of use should be 95%. In order to avoid oxygen tensions less than 55 mmHg which would increase the risk of pulmonary vasoconstriction, however, the lower limit should be 87%. Infants with indwelling arterial lines during their first few weeks of treatment should have oxygen tension measurements and simultaneous oxygen saturation readings plotted on a graph at the bedside. The graph should be updated every 48 h to take into account changed levels of 2,3-diphosphoglycerate, haemoglobin F, and carboxyhaemoglobin and the recommended limits should be changed accordingly.
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PMID:Guidelines for the use of pulse oximetry in the non-invasive estimation of oxygen saturation in oxygen-dependent newborn infants. 314 63

Blood gas and acid base values in cord blood are not predictive for neonatal cardiopulmonary adaptation on the extrauterine life. The oxygen-cardiorespirography shows objectively the state of adaptation. By this monitoring beat-to-beat heart rate, respiratory rate, thoracic impedance and the transcutaneous PO2 are measured. 16 of 337 newborns had severe cardiopulmonary problems (11 respiratory distress, 5 congenital heart disease), which was seen in at least one of the parameters. In 10 of 16 infants a pathological pattern was recognized by oxygen-cardiorespirography before clinical symptoms appeared. Additional information can be given by the hyperoxia test to differentiate healthy and sick newborns (respiratory problems and congenital heart disease). With two tcPO2-electrodes fixed on the thorax and abdomen, the shunt through an open ductus arteriosus can be estimated by different values.
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PMID:[Non-invasive monitoring of the cardiopulmonary status of newborn infants immediately following birth]. 399 Jan 52

Among 1 186 neonates admitted consecutively to the Post-Royal intensive care Unit, 203 had respiratory distress, a chest roentgenogram typical of delayed resorption of lung fluid, and no other findings. Mean gestational age (GA) was 33 weeks and mean birth-weight (BW) was 1 948 g. Hood oxygen alone was used in 129 cases and intubation-ventilation-PEEP in 74 cases (46 of which were intubated before admission). The occurrence of radiological features was similar in ventilated and non-ventilated neonates : ground-glass pattern (70-80% of the cases), increased vascular markings (70-76%) enlarged right fissure (45%), thin lateral pleural density (24%) and normal cardio-thoracic ratio. The analysis of other prognostic factors showed that ventilated neonates had a significantly lower birth weight (1 689 g versus 2 097 g) and a significantly younger gestational age (31.9 versus 33.6). The study of DAa02 in non-ventilated neonates demonstrated wide individual variations, and the possibility of an early normal DAa02 but also of a late abnormal DAa02, with the associated risks of early hyperoxia or prolonged oxygen needs. In ventilated neonates, the mean duration of intubation was 4 days 13 hours; this duration decreased as the birth-weight rose. In view of the major role of BW and GA, the Port-Royal team advocates the direct admission to a neonatal intensive care unit of neonates with delayed resorption of lung fluid and a BW under 2 000 g. In this way, Pa02 can be closely monitored and artificial ventilation is readily available.
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PMID:[Clinical and radiological findings in 203 cases of delayed resorption of pulmonary fluid (author's transl)]. 628 85

The effects of breathing greater than 95% oxygen from birth for 48 h of life on surfactant phosphatidylcholine synthesis and secretion, as well as uptake and stability of exogenous phosphatidylcholine were studied using rabbit lung tissue slices. Lung slices from animals breathing greater than 95% oxygen for 48 h exhibited a decreased rate of [14C]phosphatidylcholine release (30%) in comparison to lung slices from air-exposed controls. In vitro incorporation of [14C]choline into phosphatidylcholine was decreased by a similar amount in lung slices from pups exposed to greater than 95% oxygen. Uptake of exogenous [14C]phosphatidylcholine by lung slices from hyperoxic-exposed and control groups was not different, and the stability of extracellular phosphatidylcholine was likewise unaffected by hyperoxia. Turnover of labelled phosphatidylcholine taken up by tissue slices from medium was apparently decreased in association with hyperoxic exposure. These results are consistent with multiple sites of effect of hyperoxia on the pulmonary surfactant system in the newborn. These effects of hyperoxia on the lung surfactant system occur at a time of critical adaption to extrauterine life, and thus may have major consequences on lung function and ultimate survival of the premature infant with respiratory distress syndrome.
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PMID:Effect of hyperoxia on phosphatidylcholine synthesis, secretion, uptake and stability in the newborn rabbit lung. 648 44

Hyperoxia-mediated pulmonary damage may involve formation of toxic oxygen species such as superoxide, hydrogen peroxide, and hydroxyl radical. Intact red cells evidently scavenge these when insufflated in small numbers into the tracheobronchial tree of rats. Such manipulation protects hyperoxic rats for prolonged periods of time and preserves normal pulmonary histology. Of several potential oxygen metabolite scavengers, a role for red cell glutathione seems particularly likely. It has not escaped our attention that an ironic, and previously unsuspected, connotation of our results emerges: namely, that a small degree of spontaneous alveolar bleeding, which is not an uncommon feature in respiratory distress situations, may actually be beneficial to patients--particularly those ventilated with excessive inspired oxygen concentrations. If confirmatory studies from other laboratories are forthcoming, the tracheal insufflation of autologous red cells in ventilated patients might be considered in the future.
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PMID:Insufflated red cells protect lungs from hyperoxic damage: role of red cell glutathione in scavenging toxic O2 radicals. 653 51

Twenty preterm infants in respiratory distress, each with an umbilical catheter in place, were studied during their first 24 h of hospitalization, to determine the effects of continuous transcutaneous oxygen (PtcO2) monitoring on the frequency of arterial blood gas (ABG) determinations and on the incidence of hypoxia and hyperoxia. PtcO2 was measured continuously in all infants during the 24-h period. By random allocation, PtcO2 data were withheld during either the 1st or 2nd 12-h period of hospitalization from clinicians caring for the infant. Comparison of the 12-h period in which PtcO2 data were available (open TcM) with the period in which they were withheld showed no difference in the number of ABG determinations (6.3 +/- 0.6 vs 7.4 +/- 1.0/12 h). During the open TcM period, there was significantly less hypoxia (PtcO2 less than 50 torr) (9.0 +/- 3.7% vs 16.3 +/- 4.2%, p less than .025) but no difference in hyperoxia (PtcO2 greater than 100 torr). Although continuous PtcO2 monitoring in acutely ill newborns did not decrease the frequency of ABG determinations, it may lessen morbidity by decreasing the amount of hypoxia infants experience while being stabilized early in hospitalization.
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PMID:Continuous transcutaneous oxygen monitoring in acutely ill preterm infants. 669 30

Ten neonates with respiratory distress requiring mechanical ventilation and supplemental oxygen were studied during a continuous 24-h period to determine the value of continuous transcutaneous oxygen (PtcO2) monitoring. All 10 infants were continuously monitored during the study with a Clark-type skin electrode (Litton) and 5 of the 10 also had a catheter-tip oxygen electrode in place in the umbilical artery to measure umbilical artery O2 (PuaO2). The results of these two forms of monitoring were not available for the care of the infant during the study period. Hypoxia, as defined by a PO2 of less than 50 torr, occurred for an average of 237 +/- 51 min/24 h from continuous PtcO2 monitoring as compared with 146 +/- 33 min/24 h by estimation from arterial blood gas (PaO2) (p less than 0.05). Hyperoxia, a PO2 of greater than 75 torr, occurred 69 +/- 16 min/24 h in the continuous group and 113 +/- 26 min/24 h from PaO2 estimations. Severe hypoxia, a PO2 of less than 30 torr, was not observed from PaO2 estimations, but was seen for an average 32 +/- 15 min/24 h from the PtcO2 monitoring. These latter differences were not significant. Correlation between PaO2 and PtcO2 values (r = 0.93) was greater than the correlation between PaO2 and PuaO2 (r = 0.81). PtcO2 = 19.7 +/- 0.74 X PuaO2, and the correlation coefficient between PtcO2 and PuaO2 was 0.64. Continuous oxygen monitoring revealed significantly longer periods of hypoxia than that observed from blood gas estimations alone and its use in the low birth weight infant should result in more rational ventilatory therapy and in fewer episodes of hypoxia.
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PMID:Continuous transcutaneous oxygen monitoring in the critically ill neonate. A controlled clinical trial. 698 56

Specific changes in composition and content of lung extracellular matrix (ECM) proteoglycans (PGs) and hyaluronan (HA) have been observed during the acute response to damage in several forms of injury including infant respiratory distress syndrome (IRDS). These ECM components are thought to modulate the healing response. Hyperoxia, a contributing factor to IRDS, is known to damage both adult and developing lung, however, the extent and pattern of impairment depends on lung maturity. We hypothesized that exposing neonatal rats to hyperoxia alone might result in changes in lung HA, as well as in age-specific changes in lung PGs, similar to those shown to occur in IRDS. In control rats, lung HA decreased over the first 10 days of life, whereas rats exposed to hyperoxia exhibited a time-dependent, time-limited increase in both lung HA and lung wet weight. Histochemistry showed the HA in hyperoxia-exposed lungs to be accumulated in perivascular cuffs of medium sized arteries, and in the alveolar walls. Rats were then exposed to normoxia or hyperoxia for 7 days beginning at either 3 days of life (neonatal) or 21 days (adolescent), and lung tissue was cultured in the presence of [35S]-sulfate to label newly synthesized PGs. Proteoglycans were extracted, and analyzed by isopycnic CsCl gradient centrifugation, sequential enzymatic deglycosylation, size chromatography, and sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). When controlled for total protein extracted, 63% more label was incorporated into large molecular weight material in the tissue exposed to hyperoxia, with a 95% increase in incorporation in the most dense fraction, D1. [35S]-Sulfate incorporation into chondroitin and dermatan sulfate in hyperoxic tissue specifically increased 116% (242% in the D1 fraction), while incorporation into heparan sulfate remained essentially unchanged. There was a nearly fivefold increase in [35S]-sulfate incorporation into chondroitin sulfate chains in the D1 fraction. When the D1 fractions of extracts of treated and control rat lungs were compared on SDS-PAGE, a large chondroitin sulfate proteoglycan (CSPG; core protein of 195 kDa) was upregulated in the D1 fraction from hyperoxic tissue of neonatal rats, but was not detected in the lungs of adolescent animals exposed to hyperoxia. This CSPG and four additional large CSPGs were noted to be upregulated on western blotting by a polyclonal antibody directed against the G1 domain of the aggrecan protein core. We conclude that hyperoxia alone causes an increase in lung HA and lung water, and speculate that this contributes significantly to the clinical syndrome of IRDS. In addition, several large CSPGs are upregulated by hyperoxic exposure in a developmentally specific manner. We speculate that this increase in CSPGs may interfere with the normal developmental sequence of events, contributing to hypoalveolarization.
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PMID:Hyperoxia alone causes changes in lung proteoglycans and hyaluronan in neonatal rat pups. 757

The activity of peripheral chemoreceptors was studied in 19 preterm very low birthweight infants at the postconceptional age of 36 and 40 weeks using the hyperoxic test. The infants were in a healthy condition and did not receive any extra oxygen or medication when tested. The inhalation of pure oxygen caused a decrease in mean (SE) ventilation by 16.1 (2.6)% and 15.1 (2.1)% at the 36th and 40th gestational week respectively. At the 36th gestational week the ventilatory response was significantly slower than at 40 weeks (10.9 (6) and 7.3 (3) sec). Six infants who had been on supplemental oxygen for more than 21 days (from 21 to 56 days) responded with significantly lower response to hyperoxia at the 36th gestational week (-7.9 (3.6)%) than those receiving oxygen treatment for a shorter period of time, 0 to 16 days (-19.9 (3.2)%). The 'low responding' group included three infants who had suffered from chronic lung disease. Those infants showed the lowest hyperoxic response (-4.3 (3.9)%). There was no difference in the response among healthy preterm infants (eight infants) and infants with respiratory distress syndrome. At the 40th gestational week the differences, even though showing the same characteristics, were not statistically significant. No statistically significant relationship was found between the strength of the ventilatory response to oxygen versus gestational, postnatal age, nor the time interval between the termination of supplemental oxygen treatment and the test. No relationship was found between the number of apnoeic/bradycardic spells and the strength of the ventilatory depression caused by hyperoxia. In conclusion we found that the very preterm infants, with the exception of those who received long periods of oxygen treatment, have stronger peripheral chemoreceptor responses than those reported for 2-4 day old full term infants. However, infants who had suffered from chronic lung disease show a depressed hyperoxic response.
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PMID:Hypoxic ventilatory defence in very preterm infants: attenuation after long term oxygen treatment. 815 20

We investigated the effects of hyperoxia on the activities of hepatic ethoxyresorufin O-deethylase (EROD) (CYP1A1), methoxyresorufin O-demethylase (MROD) (CYP1A2), and glutathione transferase-alpha (GST-alpha), and the status of protein thiols (PSH) in male Sprague-Dawley rats. Twenty-four h of hyperoxia more than doubled EROD and MROD activities, which were increased 7.6- and 3.3-fold, respectively, after 48 h of hyperoxia. The increases in EROD and MROD activities were paralleled by enhanced CYP1A1/1A2 apoproteins contents, as detected by Western analysis. At 60 h of hyperoxia, by which time hyperoxic Sprague-Dawley rats display marked respiratory distress, pulmonary edema, and other markers of pulmonary dysfunction, the activities and levels of hepatic CYP1A1 and 1A2 had declined dramatically and returned to levels observed in air-breathing control animals. Hepatic activities of GST-alpha, as well as PSH status, were not altered significantly in the hyperoxic animals at any time point. The marked induction and subsequent decline of hepatic CYP1A1/1A2 activities in rats exposed to hyperoxia suggest that these enzymes may contribute to the mechanisms of injury and/or to adaptive responses to hyperoxic exposures in vivo.
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PMID:Induction and decline of hepatic cytochromes P4501A1 and 1A2 in rats exposed to hyperoxia are not paralleled by changes in glutathione S-transferase-alpha. 902 Apr 4


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