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

Continuous positive airways pressure treatment by a face chamber in idiopathic respiratory distress syndrome. During a 3-year period 45 infants with idiopathic respiratory distress syndrome (IRDS) requiring ventilatory support were treated in the neonatal unit. Continuous positive airways pressure (CPAP) via the face chamber was applied as initial therapy in 39 infants and during weaning from initial intermittent positive pressure ventilation (IPPV) treatment in 5 infants, whereas 1 infant received IPPV only. Among the 39 infants initially treated with CPAP 9 required IPPV as well. The overall survival rate was 37/45 or 82%. Incapacity to hyperoxygenate while breathing 100% oxygen was the indication for CPAP while occurrence of apnoeic attacks was the indication for IPPV. Pao2 during the hyperoxia test before ventilatory support was less than 50 mmHg in 10 infants and between 50 and 105 mmHg in 35 infants. Surviving infants were followed up with neurological and developmental control examinations as well as chest x-ray, and in several infants pulmonary function tests. 3/37 infants had moderate neurological sequelae and only 1/37 infants developed bronchopulmonary dysplasia. No deleterious effects of the face chamber were seen. As the face chamber is a noninvasive and easily applied technique for CPAP therapy without hazards, it is proposed that it should be used at a still earlier stage of IRDS in order to lesson the need for IPPV treatment and to increase the neurological and lung functional quality of survival.
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PMID:Continuous postive airways pressure treatment by a face chamber in idiopathic respiratory distress syndrome. 78 73

Prolonged exposure to hyperoxia can result in significant lung injury and has been associated with the development of bronchopulmonary dysplasia. Leukotrienes (LT) recruit polymorphonuclear leukocytes (PMN) to the lung, increase vascular permeability, and have therefore been postulated to play a role in the pathogenesis of hyperoxic lung injury. This study investigates ICI 198,615 (ICI), an LTD4 and LTE4 receptor antagonist in preventing hyperoxic lung injury in newborn rabbits. Matched littermates of 7-day-old rabbits received ICI (0.1 or 1.0 microM/kg/h) or vehicle alone, were exposed to greater than 95% O2, and sacrificed after 48, 72, 84 and 96 h of exposure. Bronchoalveolar alveolar lavage fluid (BAL) of the left lung was analyzed for white cell count, differential, absolute number of PMNs, total protein, and cyclooxygenase products 6-keto-PGF1 alpha, and thromboxane B2. Lung water was quantified utilizing the right lung. Results demonstrated no significant differences between the ICI groups or between the ICI groups and controls. In conclusion, the administration of the LTD4 and LTE4 receptor antagonist ICI 198,615 was insufficient to reduce the formation of pulmonary edema, reduce mortality or attenuate hyperoxic lung injury. These experiments suggest that a number of other mediators may be involved in the hyperoxic lung injury process and that the functional inhibition of a portion of the arachidonic acid cascade was not sufficient to either prevent or attenuate hyperoxic lung injury in newborn rabbits.
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PMID:Evaluation of a leukotriene receptor antagonist in prevention of hyperoxic lung injury in newborn rabbits. 131 78

The immaturity of the lung of the very prematurely delivered newborn appears to make it hypersusceptible to injury by those very therapeutic measures that the infant requires shortly after birth--mechanical ventilation and hyperoxia. There is good experimental evidence to relate the immature lung's susceptibility to early hyperoxia-induced lung damage to deficient antioxidant defensive systems. Less than fully adequate nutritional support of these tiny newborns can have extremely detrimental effects on their lungs' ability to resist and repair on-going injury and to continue developing normally. Promising experimental means of possible protection from hyperoxic lung damage and progression to chronic lung disease (bronchopulmonary dysplasia) are reviewed.
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PMID:Antioxidants, nutrition, and bronchopulmonary dysplasia. 152 71

Steady-state levels of mRNAs for the three surfactant-associated proteins, SP-A, SP-B, and SP-C, were measured in a primate model of premature birth and survival. These values were determined by Northern and quantitative slot blot analyses of total lung RNA during both in utero and extrauterine development of the fetus as well as in response to hyperoxic exposure. The composition and surface properties of surfactant were also analyzed to determine the effect of differential expression of the surfactant proteins on the overall composition and function of surfactant. The data clearly demonstrate that the regulation of surfactant mRNA levels in the premature fetus is under complex physiological control. Interruption of in utero development by premature birth results in increased levels of all three surfactant mRNAs, presumably in response to precocious initiation of air breathing. Within the first 24 h after parturition both SP-B and SP-C mRNA levels are increased beyond the levels found in the full-term fetal controls. Expression of mRNA for these genes peaks on day 2 and thereafter drops to levels below that found on day 1. However, response of the SP-A gene to premature birth is slow and transcripts from this gene lag considerably behind values found in the full-term fetus. Furthermore, exposure of the premature fetus to hyperoxia results in an increase in the steady-state levels of SP-B and SP-C mRNA without significant changes in SP-A. Defects in the ability of the SP-A gene to respond to extrauterine exposure and hyperoxia may be contributing to development of bronchopulmonary dysplasia, a common clinical complication of premature birth in humans.
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PMID:Alterations in surfactant protein gene expression associated with premature birth and exposure to hyperoxia. 176 59

Microbial colonization and infection patterns were prospectively evaluated in premature baboons with and without bronchopulmonary dysplasia (BPD) to assess if prolonged hyperoxia would predispose to a different pattern of microbial colonization and/or a higher risk of respiratory infection. Forty baboons were delivered by hysterotomy at 75% of gestation and randomized into two groups. Group I (control or PRN) animals were placed immediately on high-frequency oscillation at 15 Hz; I:E ratio 1:2, and changed to positive-pressure ventilation at 48 to 72 h. They were maintained on clinically appropriate oxygen at minimal ventilator settings for the remainder of the 21-day experimental period. Group II (oxygen-treated or BPD) animals were ventilated with PPV and FIO2 1.0 for 7 days followed by FIO2 0.8 for 14 days. All animals were treated with antibiotics during some portion of the 21-day course. Specimens from nose, oropharynx, trachea, and rectum were cultured for both aerobes and anaerobes throughout the neonatal intensive care unit (NICU) course. A subset of animals from both groups were killed at 21 days and lung, liver, spleen, and gastric contents were cultured quantitatively at autopsy. Findings showed that coagulase-negative staphylococci were the predominant organisms that colonized the neonate in the NICU. Lung infections were seen to evolve through sequential pathogenetic steps: colonization of the upper respiratory tract, with concomitant or subsequent colonization of the trachea with comparable organism and ultimate recovery of the same organisms at autopsy in the lungs of animals with pneumonia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bacterial colonization and infection studies in the premature baboon with bronchopulmonary dysplasia. 195 45

Although the prematurely born are known to have decreased baseline levels of protective antioxidant enzymes (Frank L, Sosenko IRS: J Pediatr 110:9 and 106, 1987), the ability to augment the baseline values during high O2 exposure is the key factor determining O2 tolerance versus O2 susceptibility. We have compared the pulmonary antioxidant enzyme responses of prematurely delivered rabbits (gestational d 29 of 32) and full-term rabbits to 48-72 h of hyperoxic exposure. We found that although full-term newborns exposed to greater than 90% O2 consistently showed elevated superoxide dismutase, catalase, glutathione peroxidase, and glucose-6-phosphate dehydrogenase activities, the premature animals repeatedly failed to respond to hyperoxia with increased antioxidant enzyme activity levels. Consistent with the comparative antioxidant enzyme responses were the evidences of O2 toxicity in the two age groups. The prematurely born rabbits had significantly increased lung lavage protein content, lung conjugated diene levels, and more severe light microscopic lung pathology compared with the full-term animals during equal O2 exposure time. This first reported comparison of prematurely born versus full-term animal responses to hyperoxia might help to explain the clinical observation that the very prematurely born infant is excessively prone to the development of O2-induced lung injury and the progressive development of bronchopulmonary dysplasia.
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PMID:Failure of premature rabbits to increase antioxidant enzymes during hyperoxic exposure: increased susceptibility to pulmonary oxygen toxicity compared with term rabbits. 203 78

With improved survival of critically ill premature infants, BPD has become an important sequela of neonatal intensive care. A variety of medications are used in the management of BPD. In this article we have attempted to summarize clinical efficacy, pharmacokinetics, and side effects of many of these medications. Longer-term studies on the efficacy of drug therapy are needed and may be facilitated by the development of accurate and reproducible computerized techniques for the measurement of pulmonary mechanics in neonates. Ultimately, new pharmacologic agents or other strategies that will prevent lung injury from hyperoxia and mechanical ventilation or accelerate tissue repair once injury occurs will play a major role in the prevention and treatment of infants with BPD.
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PMID:Drug therapy for bronchopulmonary dysplasia. 219 Dec 59

Deficiencies of antioxidants and increased free radical generation may explain the high incidence of bronchopulmonary dysplasia in premature infants. Long-acting antioxidants such as polyethylene glycol (PEG) conjugated superoxide dismutase (SOD), and catalase might modify this process. We delivered 32 premature lambs, 16 pairs of twins, by cesarean section at 125-141 days of gestation (term 146 days) and stabilized them on ventilators in normocapnic hyperoxia for a period of 8 h. One lamb of each twin pair received an intravenous dose of 7,500-50,000 IU/kg of PEG-SOD and of 37,500-1,000,000 IU/kg of PEG-catalase at birth. Their siblings acted as controls. Mean airway pressure, arterial pressure, and heart rate were recorded continuously. Arterial blood gases and pH were obtained every 30 min. After sacrifice, standardized lung biopsies were prepared for quantitative morphometrics and electron microscopy. Administration of PEG antioxidants at birth reduced the influx of neutrophils and macrophages into the lung and damage to arterioles, bronchiolar mucosa, and type II pneumocytes without major changes in alveolar surface area or pulmonary function. These effects were dose-related and detectable even at the lowest doses of PEG antioxidants administered.
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PMID:Mitigation of pulmonary oxygen toxicity in premature lambs with intravenous antioxidants. 235 45

Immaturity, pulmonary barotrauma, and oxygen toxicity have been implicated in the pathogenesis of bronchopulmonary dysplasia (BPD). Although the physiologic and biochemical consequences of oxygen toxicity have been described in newborn and adult animals, there have been no controlled observations in prematures. We compared the physiologic and morphologic effects of prolonged hyperoxia with those of clinically appropriate oxygen in premature baboons with hyaline membrane disease (HMD) supported with conventional positive pressure ventilation and continuous distending airway pressure (PPV/PEEP). Twenty-one premature baboons were delivered at 140 days gestation, intubated and resuscitated, and supported with PPV/PEEP and standard NICU techniques for 11 days. The FIO2, PaO2, PaCO2, pHa, ventilator and airway pressures, and blood pressure were intermittently measured and recorded. The physiologic observations could be divided into 3 distinct phases. During Phase 1 (0 to 42 h) there were no significant intergroup differences, and (a/A)PO2 and IO2 (oxygenation index; (a/A)PO2/Paw) remained stable. In Phase 2 (43 to 96 h) there was a rapid improvement in (a/A)PO2 and IO2 in both groups, but the response in the hyperoxic animals was significantly dampened. During Phase 3 (97 to 264 h) there was continued improvement in the "prn" animals, which contrasted with progressive deterioration in those exposed to FIO2 1.0. Five of 11 "prn" and 3 of 10 FIO2 1.0 baboons developed air leaks during Phase 1 or early Phase 2. Four of 10 of the hyperoxic animals died after the late onset of air leak. Pathologic changes of BPD were found in all FIO2 1.0 animals surviving more than 6 days but in none of the "prn" long-term survivors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oxygen toxicity in the premature baboon with hyaline membrane disease. 330 71

In summary, the pulse oximeter provides a reliable, continuous assessment of oxygenation in newborn infants. Its rapid response time and ease of use make it a practical device for use on all sick newborns. To avoid hyperoxia it should be used in conjunction with arterial blood gas measurements and we recommend a high SaO2 alarm of 92% in infants with predominantly fetal hemoglobin. Finally, it is an improved way of monitoring oxygenation in very immature infants and in infants with bronchopulmonary dysplasia.
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PMID:Pulse oximetry--an alternative to transcutaneous PO2 in sick newborns. 367 56


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