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

Bronchopulmonary dysplasia (BPD) is one of the most significant sequelae of prematurity, affecting the pulmonary and cardiovascular structures especially. From the first weeks of life, there exists a close anatomical and functional relationship between these two systems. Changes in intrathoracic pressure or pulmonary vascular resistance greatly impact both the left and right sides of the heart. In turn, increasing afterload and decreasing preload affect blood flow through the lung, as well as the state of oxygenation and ventilation. BPD affects the function, growth, and development of the heart and lung, due to the hypoxia, acidosis, hyperoxia, and fibrosis associated with the fibroproliferative repair process. Significance of clinical findings and the role of the bedside caregiver are also discussed.
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PMID:Bronchopulmonary dysplasia: its effects upon the heart and lungs. 942 48

It has previously been reported that active glottic adduction is present during prolonged apneas but absent during periods of breathing movements in fetal lambs in utero. The present study was aimed at examining the precise coordination between fetal breathing movements [diaphragm electromyographic (EMG) activity (Di EMG)] and glottic adduction [thyroarytenoid muscle EMG activity (TA EMG)]. Electrodes for electroencephalogram, eye movements, TA EMG, and Di EMG and an arterial catheter were surgically implanted in fetal lambs 123-142 days postconception. Polygraphic recordings were performed without sedation while the ewe breathed room air (n = 11) or various gas mixtures (hypoxia, n = 5; hyperoxia, n = 4; hypercapnia, n = 5; hypercapnia+hyperoxia, n = 5). Tonic TA EMG was observed throughout >90% of apneas (>6 s) in both non-rapid-eye-movement and rapid-eye-movement sleep, and when Di EMG frequency decreased in rapid-eye-movement sleep. In all but two fetuses, TA EMG was immediately inhibited when Di EMG appeared. Altering blood gases did not modify these results. In conclusion, Di EMG and TA EMG are well coordinated in late gestation in fetal lambs, except in a few cases. These findings may have consequences for understanding the pathogenesis of mixed/obstructive apneas of prematurity.
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PMID:Coordination between glottic adductor muscle and diaphragm EMG activity in fetal lambs in utero. 957 99

Chronic lung disease (CLD) of prematurity may be caused by a number of insults during mechanical ventilation, including barotrauma and hyperoxia. To evaluate bronchial hyperresponsiveness (BHR) in infants with CLD of prematurity, we measured changes in transcutaneous oxygen tensions (tcPO2) during methacholine inhalation challenge. Twelve infants with CLD and 22 age-matched children without respiratory diseases were enrolled in this study (ages--5 to 36 months; mean age--16.2 months). Serial doses of methacholine were doubled until a 10% decrease in tcPO2 from baseline was reached. The cumulative dose of methacholine inhaled by the time tcPO2 had been reached (Dmin-PO2) was considered to represent the dose at which reactivity to methacholine (RO2meth) had occurred. In the CLD group, Dmin-PO2 (3.50 +/- 0.1 log x milli-units) was significantly lower than in the preterm control infant group (4.31 +/- 0.2 log x milli-units) and the term infant group (4.21 +/- 0.1 log x milli-units) (P = 0.004, P < 0.001). Dmin-PO2 in the preterm control infant group was not significantly different than in the term infant group (P > 0.5). These results suggest that infants who require additional therapeutic oxygen and mechanical ventilation during the early months of life are at risk of developing early-onset, long-lasting respiratory disease that is related to an acquired BHR.
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PMID:Transcutaneous oxygen tension measurements during methacholine challenge of prematurity in infants with chronic lung disease. 963 36

The imbalance between high oxidant loads and immature antioxidant defenses is associated with long-term complications of prematurity. Glutathione is a central element among the antioxidants. Depletion of pulmonary glutathione accelerates the development of oxygen-induced lung injury in neonatal animal models. After the observation that newborn infants exposed to oxygen have low glutathione levels, a study was designed to test the hypothesis that in neonates from a species susceptible to oxygen toxicity, the lethal effect of hyperoxia is related to a low availability of substrates for glutathione production rather than an impairment in synthetic activity. One-day-old guinea pigs, randomly assigned to room air or oxygen (>95%), were fed by their mothers (n = 16) or i.v. by dextrose (n = 14) or by total parenteral nutrition (TPN, n = 20). After 3 d, glutathione and activities of enzymes involved in maintaining intracellular glutathione levels were determined in lungs and liver. The lethal effect of oxygen (p < 0.05) observed in animals without TPN was not related to glutathione depletion, as oxygen induced a 33% increase in lung glutathione, positively correlated (r2 = 0.35) with enhanced synthesis. With TPN, the animals were protected against the lethal effects of hyperoxia and lung glutathione increased by 67% in oxygen. The results suggest that the glutathione demand by the lungs in the presence of an oxidant stimulus was met by the increased (p < 0.001) hepatic production supported by TPN. Under hyperoxic conditions, early nutritional support is of vital importance.
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PMID:Survival of guinea pig pups in hyperoxia is improved by enhanced nutritional substrate availability for glutathione production. 1047 45

Retinopathy of prematurity (ROP) is a major problem in both highly developed countries and countries with emerging technology. The incidence of ROP has been stable over the last 2 decades despite improvements in neonatology. Threshold ROP occurs in about 5% of premature infants in the US with birthweights <1.25kg. Despite treatment, a sizable minority will become blind (up to 20 to 30%). The pathophysiology of ROP can be separated into 2 phases. Phase I is hyperoxia-vasocessation. Phase II is hypoxia-vasoproliferation. The former occurs immediately following premature birth. The provision of supplemental oxygen causes retinal hyperoxia, a down regulation of vascular endothelial growth factor (VEGF) and a consequent cessation of normal retinal vascularisation. Systemic factors and increasing retinal metabolic demands cause a shift to phase II when a relative retinal hypoxia develops. This hypoxia stimulates VEGF production, leading to renewed vascularisation. This can be the resumption of normal vascularisation or abnormal neovascularisation, depending on local retinal responses. The management of ROP begins with a reliable evidence-based screening protocol. All interested parties must cooperate in developing and implementing foolproof screening protocols. Hospital officials, nursery personnel, neonatologists and ophthalmologists all have areas of responsibility in ensuring adequate screening. ROP management involves prevention, interdiction and correction. Prevention includes: adequate prenatal care which minimises premature birth, and appropriate systemic intensive care which lessens the tissue hyperoxia/hypoxia swings. Pharmacological vitamin E supplementation has largely been abandoned and ambient light reduction has been shown to be ineffective. The value of inositol supplementation and angiogenesis inhibitors in preventing ROP is presently under investigation. Interdiction concentrates on ablation of the peripheral avascular retina, thus dramatically decreasing VEGF production. Both cryotherapy and laser photocoagulation are effective; however, unfortunately, poor outcomes persist despite treatment. Supplemental oxygen administration has so far proven ineffective in limiting ROP progression. Finally, correction focuses on vitrectomy/retinal detachment repair. While anatomically successful, this procedure is often unsuccessful in terms of restoration of vision (<5% success rate). In conclusion, despite improvements in neonatology, ROP, potentially leading to blindness, continues to be a common problem associated with prematurity. Future management success must concentrate on discovering new modes of treatment, especially prevention.
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PMID:The management of retinopathy of prematurity. 1135 98

Newborn infants may be transferred to a special care nursery because of conditions such as prematurity (gestation less than 37 weeks), prolonged resuscitation, respiratory distress, cyanosis, and jaundice, and for evaluation of neonatal sepsis. Newborn infants' core temperature should be kept above 36.4 degrees C (97.5 degrees F). Nutritional requirements are usually 100 to 120 kcal per kg per day to achieve an average weight gain of 150 to 200 g (5 to 7 oz) per week. Standard infant formulas containing 20 kcal per mL and maternal breast milk may be inadequate for premature infants, who require special formulas or fortifiers that provide a higher calorie content (up to 24 kcal per mL). Intravenous fluids should be given when infants are not being fed enterally, such as those with tachypnea greater than 60 breaths per minute. Hypoglycemia can be asymptomatic in large-for-gestational-age infants and infants of mothers who have diabetes. A hyperoxia test can be used to differentiate between pulmonary and cardiac causes of hypoxemia. The potential for neonatal sepsis increases with the presence of risk factors such as prolonged rupture of membranes and maternal colonization with group B streptococcus. Jaundice, especially on the first day of life, should be evaluated and treated. If the infant does not progressively improve in the special care nursery, transfer to a tertiary care unit may be necessary.
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PMID:Common issues in the care of sick neonates. 1244 67

The basic mechanism of kernicterus and bilirubin encephalopathy has not been unequivocally determined. Much knowledge has been gained about phenomena that contribute to bilirubin neurotoxicity, and this knowledge has implications for clinical practice. Conditions that impact on blood-brain barrier function, increase brain blood flow, or impact on bilirubin metabolism, including its transport in serum, should be avoided, if possible. Such conditions include drugs and drug stabilizers that compete with bilirubin binding to albumin, or that inhibit P-glycoprotein in the blood-brain barrier, prematurity/immaturity, and clinically significant illness in the infant that involves hemolysis, respiratory and metabolic acidosis, infection, asphyxia, hypoxia and (perhaps) hyperoxia, and hyperosmolality. If these conditions are not avoidable then there should be a more aggressive approach to the treatment of hyperbilirubinemia. The limits of tolerance for hyperbilirubinemia varies among neonates and there are no tools to determine with certainty when a particular infant is approaching the danger zone. Neurological symptoms in a jaundiced infant require extreme vigilance, and, in most cases, immediate intervention.
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PMID:Mechanisms of bilirubin toxicity: clinical implications. 1251 45

The development of Chronic Lung Disease of Prematurity (CLD) has been associated with the use of hyperoxic conditions during ventilation. Inflammation has been demonstrated to contribute to the development of this disease, both on histological examination of diseased lungs, and by the use of bronchoalveolar lavage. Hyperoxia is believed to contribute to this inflammatory process by causing direct injury to epithelial and endothelial cells. The formation of reactive oxygen species is thought to result in production of cytokines. These act within a complex network, orchestrating an inflammatory response. Evidence for a role of cytokines in CLD has been inferred by studies in human infants showing increased concentrations of cytokines, growth factors and inflammatory cells at early stages in infants destined to develop CLD. These findings have been supported by the use of animal models of hyperoxic lung injury. The treatment of CLD is currently centered on the suppression of cytokine production. As understanding of this disease increases, more specific targets are being developed which aim to reduce the oxidative load on the lung, and prevent recruitment of inflammatory cells that are responsible for the tissue damage underlying this disease.
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PMID:Role of cytokines in hyperoxia mediated inflammation in the developing lung. 1270 Jan 33

The opportunities for very low birth weight infants (birth weight < 1500 g) and extremely low birth weight infants (birth weight < 1000 g) to undergo surgery are increasing. These infants are prone to prematurity-related morbidities including respiratory distress syndrome, intraventricular haemorrhage, periventricular leukomalacia, retinopathy of prematurity, patent ductus arteriosus and necrotising enterocolitis. Evidence is accumulating that preterm infants are also sensitive to pain and stress. The pharmacokinetics of drugs in preterm infants is not fully understood but smaller doses of anaesthetic drugs are usually required in preterm infants compared to term infants and older children and their effects last longer due to low clearance rates and longer elimination half-lives. Key anaesthetic considerations are (i) inspired oxygen concentration that should be adjusted to avoid hyperoxia, (ii) haemodynamic parameters that should be kept stable and (iii) prevention of hypothermia by using adequate measures to keep the infants warm. These precautions must be continuously taken during the operation and the transport to and from the operating theatre.
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PMID:Anaesthetic considerations for the management of very low and extremely low birth weight infants. 1517 4

To examine whether prematurity significantly changes the lung inflammatory response to oxygen, rabbit lung explant cultures were exposed to 95% or 5% oxygen for 24 hours. Interleukin (IL)-8 protein concentrations from homogenates of the premature lung rose significantly after hyperoxia (6.8 +/- 1.8 in 5% O2 to 45.7 +/- 21.3 pg/microg protein in 95% O2) but not in the term lung (15.9 +/- 6.7 to 20.4 +/- 4.3 pg/microg protein). There was no change in IL-8 mRNA after hyperoxia in either age group. Preterm lungs demonstrated higher IL-8 levels by fluorescence-activated cell sorting (FACs) analysis and immunohistochemistry. This model may help determine why premature lungs are more susceptible to oxygen-induced disease.
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PMID:Effect of hyperoxia on interleukin-8 expression in premature versus term rabbit lung explants. 1520 34


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