bronchopulmonary dysplasia/edema

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Excessive gas exchange impairment during exercise in a subject with a history of bronchopulmonary dysplasia and high altitude pulmonary edema.

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A 27-year-old male subject (V(O2 max)), 92% predicted) with a history of bronchopulmonary dysplasia (BPD) and a clinically documented case of high altitude pulmonary edema (HAPE) was examined at rest and during exercise. Pulmonary function testing revealed a normal forced vital capacity (FVC, 98.1%

Bronchopulmonary dysplasia: possible relationship to pulmonary edema.

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The pathogenesis of bronchopulmonary dysplasia is controversial. Oxygen toxicity, mechanical trauma to the lung secondary to respirator therapy, and congestive heart failure with a left to right shunt through a patent ductus arteriosus have all been implicated. Our data suggest that in addition to

Normal pulmonary vascular resistance and left ventricular hypertrophy in young infants with bronchopulmonary dysplasia: an echocardiographic and pathologic study.

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To evaluate the cardiac anatomy and functional hemodynamics in young infants with chronic lung disease, nine patients, aged 2 to 7 months, with a clinical diagnosis of bronchopulmonary dysplasia (BPD) underwent echocardiographic examination. All infants required supplemental O2 (mean FIO2 35%) to

[Expression of high mobility group protein-B1 in mice with hyperoxia-induced bronchopulmonary dysplasia].

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OBJECTIVE To study the effect of hyperoxia exposure on high mobility group protein-B1 (HMGB1) expression in neonatal mice and the role of HMGB1 in the pathogenesis of bronchopulmonary dysplasia (BPD). METHODS C57BL/6 mice were randomly exposed to 60% O2 or air 1 day after birth. BPD was induced by

[Bronchopulmonary dysplasia].

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Bronchopulmonary dysplasia is a most frequent contemporary lesion of the lung in early childhood. It is characterized by clinical symptoms (neonatal respiratory distress syndrome) and by X-ray picture reflecting progressive morphological changes in the respiratory tract, i.e. in trachea, bronchi,

Deep Illumina sequencing reveals differential expression of long non-coding RNAs in hyperoxia induced bronchopulmonary dysplasia in a rat model.

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BACKGROUND Bronchopulmonary dysplasia (BPD) in premature infants is a predominantly secondary occurrence to intrauterine inflammation/infection and postpartum mechanical ventilation; The purpose of this study is to explore the biological roles of lincRNA in the pathogenesis of BPD. METHODS Newborn

Dexamethasone does not affect vasopressin release in bronchopulmonary dysplasia.

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Elevated levels of vasopressin (AVP) have been found in premature infants with bronchopulmonary dysplasia (BPD), and may be related to abnormalities of water handling, and to non-pulmonary signs of edema. Dexamethasone treatment improves pulmonary function in infants with BPD, and is frequently

Expression and activity of epithelial sodium channel in hyperoxia-induced bronchopulmonary dysplasia in neonatal rats.

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BACKGROUND The aim of the present study was to investigate the expression and activity of epithelial sodium channel (ENaC) in hyperoxia-induced bronchopulmonary dysplasia (BPD) in neonatal rats. METHODS Neonatal rats were exposed to hyperoxia to establish BPD models (control group was exposed to

Placental Chorioangioma with Nonimmune Hydrops Fetalis.

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A 38-year-old woman was found to have a large placental chorioangioma. The fetus was studied using ultrasound. The pregnancy became complicated by hydrops fetalis, polyhydramnios, and abruptio placenta. The infant delivered at 29 weeks' gestational age. The neonatal course was complicated by

Bronchodilators and diuretics in children with bronchopulmonary dysplasia.

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Pulmonary function tests (PFT) were obtained during the course of a self-controlled study of six children aged 5 to 43 months who had moderate to severe bronchopulmonary dysplasia (BPD). Changes after the administration of intravenous (IV) furosemide (2 mg/kg), inhaled isoproterenol (0.2 cc, 1:200),

Pathogenesis of bronchopulmonary dysplasia following hyaline membrane disease.

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The pathologic changes in the lungs of 112 infants dying from hyaline membrane disease (HMD) and 64 infants dying from other causes in the years 1967 to 1972 have been reviewed in order to obtain information about the pathogenesis of bronchopulmonary dysplasia (BPD). The results from the infants

Edema formation in the newborn lung.

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Pulmonary edema is an important cause of respiratory distress in newborn infants. It occurs with severe perinatal asphyxia, heart failure, hyaline membrane disease, persistent patency of the ductus arteriosus, pneumonitis from group B beta-hemolytic streptococcus, and chronic lung disease

Vasculoprotective effects of heme oxygenase-1 in a murine model of hyperoxia-induced bronchopulmonary dysplasia.

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Bronchopulmonary dysplasia (BPD) is characterized by simplified alveolarization and arrested vascular development of the lung with associated evidence of endothelial dysfunction, inflammation, increased oxidative damage, and iron deposition. Heme oxygenase-1 (HO-1) has been reported to be protective

[Bronchopulmonary dysplasia]

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OBJECTIVE: To review the literature on bronchopulmonary dysplasia. METHODS: The most important articles on bronchopulmonary dysplasia were selected through MEDLINE. RESULTS: The present review analyzes the different concepts, pathogenesis, clinical presentation, treatment and prophylaxis of

Bronchopulmonary dysplasia.

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Neonatal pulmonary diseases may require mechanical ventilation and supplemental oxygen therapy. These supportive measures can damage the immature lung or distort the normal maturation processes of the developing lung. The formation of hyaline membranes occurs acutely, often complicated by

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