25 research outputs found
Antenatal Cocaine Exposure Produces Accelerated Surfactant Maturation without Stimulation of Antioxidant Enzyme Development in the Late Gestation Rat
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NO for preterm infants at risk of bronchopulmonary dysplasia
Failure of Premature Rabbits to Increase Antioxidant Enzymes During Hyperoxic Exposure: Increased Susceptibility to Pulmonary Oxygen Toxicity Compared with Term Rabbits
Lung Development in the Fetal Guinea Pig: Surfactant, Morphology, and Premature Viability
Lung Development in the Streptozotocin Rat Fetus: Antioxidant Enzymes and Survival in High Oxygen
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Positive Regulation of Pulmonary Antioxidant Enzyme Gene Expression by Prenatal Thyrotropin Releasing Hormone Plus Dexamethasone Treatment in Premature Rats Exposed to Hyperoxia
Bronchopulmonary dysplasia: changes in pathogenesis, epidemiology and definition
Bronchopulmonary dysplasia (BPD) continues to be one of the most common long-term complications associated with preterm birth. Its incidence is increasing as the survival of extreme premature infants improves, but its clinical presentation is milder than the original description of Northway and collaborators. In contrast to the classic BPD that was strongly related to mechanical injury and oxygen toxicity, current forms of the condition are more related to immaturity, perinatal infection and inflammation, persistent ductus arteriosus and disrupted alveolar and capillary development. Many different definitions of BPD have been proposed, most of which are based on the duration of supplemental oxygen requirement. The different definitions can produce strikingly different incidence figures, which may account for the wide variations in the condition reported in the literature. Some of the limitations of the criteria most commonly used to diagnose BPD are discussed in this article