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At least 19 recordsLinked to original sources
PubMed1979

A possible role of vitamin E in the prevention or amelioration of bronchopulmonary dysplasia.

Bronchopulmonary dysplasia (BPD) is a significant cause of chronic pulmonary disease following mechanical ventilation of newborn infants. Although the exact pathogenesis of BPD has yet to be elucidated, high concentration of supplemental oxygen delivered by positive pressure through an endotracheal tube is thought to be a major predisposing factor. The only reported clinical trial of the administration of an exogenous antioxidant as vitamin E (20 mg/kg/day I.M.) to premature infants with respiratory distress syndrome who were receiving supplemental oxygen greater than 40% showed a shorter exposure to all levels of supplemental oxygen when compared to a control group. No roentgenographic changes of BPD were noted in any vitamin-E-treated infants. Vitamin E may modify the development of BPD, but until further clinical trials demonstrate a significant reduction in the incidence and severity of BPD, efforts should be made to minimize exposure to any of the associated factors in the pathogenesis of BPD.

Humans↗
PubMed2024

Improving early diagnosis of bronchopulmonary dysplasia.

INTRODUCTION: Bronchopulmonary disease (BPD) is associated with long-term neurodevelopmental and cardiorespiratory complications, often requiring significant use of resources. To reduce this healthcare burden, it is essential that those at high risk of BPD are identified early so that strategies are introduced to prevent disease progression. Our aim was to discuss potential methods for improving early diagnosis in the first week after birth. AREAS COVERED: A narrative review was undertaken. The search strategy involved searching PubMed, Embase and Cochrane databases from 1967 to 2024. The results of potential biomarkers and imaging modes are discussed. Furthermore, the value of scoring systems is explored. EXPERT OPINION: BPD occurs as a result of disruption to pulmonary vascular and alveolar development, thus abnormal levels of factors regulating those processes are promising avenues to explore with regard to early detection of high-risk infants. Data from twin studies suggests genetic factors can be attributed to 82% of the observed difference in moderate to severe BPD, but large genome-wide studies have yielded conflicting results. Comparative studies are required to determine which biomarker or imaging mode may most accurately diagnose early BPD development. Models which include the most predictive factors should be evaluated going forward.

Humans↗
PubMed2025

Adrenomedullin overexpression protects mice from experimental bronchopulmonary dysplasia and associated pulmonary hypertension.

Bronchopulmonary dysplasia (BPD) associated pulmonary hypertension (PH) or BPD-PH is a lung disease of infants with significant morbidity. Adrenomedullin (Adm) is an angiogenic peptide that signals through calcitonin receptor-like receptor (Calcrl) and receptor activity modifying protein 2 (RAMP2). Adm deficiency potentiates hyperoxia-induced experimental BPD-PH in mice; however, whether Adm overexpression can mitigate this lung disease is unclear. Thus, we tested the hypothesis that Adm overexpression attenuates hyperoxia (HO)-induced murine experimental BPD-PH by using a novel transgenic mouse that overexpresses Adm globally (Admhi/hi mice). One-day-old Admhi/hi mice or their wild-type littermates (Adm+/+ mice) were exposed to HO ([Formula: see text] 70%) for 14 days and allowed to recover in normoxia (NO, [Formula: see text] 21%) for an additional 14 days. Controls were maintained in NO for 28 days. On postnatal day (P) 14, we harvested the lungs to determine the extent of Adm expression and apoptosis. On P28, we quantified alveolarization, lung vascularization, and PH. HO-exposed Adm+/+ mice demonstrated increased lung apoptosis, decreased alveolarization and lung vascularization, and indices of PH, indicating that neonatal HO exposure causes BPD-PH. However, Adm overexpression attenuated experimental BPD-PH, as evident by the decreased extent of hyperoxia-induced lung apoptosis and inflammation, alveolar and vascular simplification, pulmonary vascular remodeling, and PH in Admhi/hi mice than in Adm+/+ mice. Collectively, our results demonstrate that Adm overexpression attenuates HO-induced murine experimental BPD-PH, emphasizing the therapeutic potential of Adm for BPD-PH in preterm infants.NEW & NOTEWORTHY The deficiency of the proangiogenic peptide, adrenomedullin (Adm), exacerbates the severe infantile lung disorder, bronchopulmonary dysplasia-associated pulmonary hypertension (BPD-PH), in mice. However, whether Adm therapy can mitigate this disease is unclear. Our study, conducted with a rigorous methodology, suggests a potential solution. Using a novel mouse that overexpresses Adm to overcome the pharmacological limitations of the peptide, we demonstrate that Adm can mitigate this disorder, highlighting the therapeutic potential of Adm for human BPD-PH.

Animals↗
PubMed1979

Bronchopulmonary dysplasia--pathology.

The term bronchopulmonary dysplasia has much to commend it. It does not declare the etiology of this disease, which seems to be an advantage. Another advantage is that it presents the idea of disturbance of growth as well as scarring. The premature lung responds at birth somewhat differently from the mature lung, not just in respect to surfactant but from the point of view of the blood vessels' size and compliance. But treatment must also be considered. The administration of steroids to the mother in the antenatal period probably favors maturation in the fetus, rather than growth of size and cell multiplication, which will also influence the behavior of the lung postnatally. This is probably a critical feature to look for in clinical assessment and follow-up of these patients.

Humans↗
PubMed2026

Inhaled vitamin A mitigates hyperoxia-induced acute and chronic lung damage in a neonatal rat model of bronchopulmonary dysplasia.

RATIONALE: Prevention of bronchopulmonary dysplasia (BPD) remains a critical unmet need. OBJECTIVES: We continued evaluating aerosolized vitamin A in a neonatal rat hyperoxia-injury model of BPD, testing whether lung-targeted inhalation yields superior outcomes compared to enteral or intramuscular (IM) delivery. METHODS: Rat pups were exposed to continuous 95% hyperoxia for seven days to induce lung damage. Vitamin A was administered from post-natal day (PD) 1-7 by inhalation, enteral or IM dosing. Persisting effectiveness of inhaled vitamin A was examined at PD 21, dwelling in normoxia after all interventions were discontinued at PD 7. MEASUREMENTS AND MAIN RESULTS: Comprehensive analyses include alveolar morphometrics, in vivo pulmonary function testing, assessment of hepatic vitamin A level, and quantitating gene and protein expression of relevant biomarkers of lung maturation, inflammation and damage/repair, employing singlex and multiplexed assays and whole-genome gene expression. CONCLUSIONS: Inhaled vitamin A suppressed hyperoxia-induced lung damage, with key hallmarks of BPD, including lung morphometrics and biomarkers associated with lung damage and inflammation, being effectively indistinguishable from healthy controls at both PD 7 and 21, Natural reparative processes were enhanced, with normal alveolarization and pulmonary function at PD 21. Despite raising hepatic vitamin A levels, enteral dosing was ineffective in restoring alveolar morphology at PD 7. Consistent with previous reporting, IM dosing yielded modest effect at PD 7 but with little evidence of benefit to pulmonary function at PD 21. Observation of dose-dependent effects with aerosolized vitamin A strengthens the evidence of the benefits of lung-targeted delivery, supporting further development of inhaled vitamin A as a BPD preventive strategy.

Journal Article↗
PubMed1978

Bronchopulmonary dysplasia: possible relationship to pulmonary edema.

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 these three conditions, all of which are edemagenic, infants with bronchopulmonary dysplasia have a significantly greater mean fluid intake in the first five days of life when compared with infants with respiratory distress syndrome or patent ductus arteriosus alone. We suggest that the addition of a fluid load may potentiate the effects of other factors and increase the risk of bronchopulmonary dysplasia in infants with respiratory distress syndrome who require respiratory support.

Bronchial Diseases↗
PubMedDate not supplied

The relationship of bronchopulmonary dysplasia to the occurrence of alveolar rupture during positive pressure ventilation.

The effect of altered mechanical ventilation on the incidence of alveolar rupture and bronchopulmonary dysplasia (BPD) was reviewed in infants who had neonatal respiratory distress syndrome (RDS) (N = 99). From 1971 to 1974 we attempted to minimize pulmonary oxygen exposure. Accordingly, during the resolution of respiratory distress syndrome, the ventilator pressures were not reduced until the FIO2 had been lowered to 0.4 (n = 61). In 1974 to 1975 earlier reduction of pressure was instituted as the FIO2 was lowered to 0.6 or less (N = 38). Birth weight and gestational age were comparable in the two groups. With earlier reduction of ventilator pressures, there was a significant decrease in the duration of exposure to peak inspiratory pressures greater than or equal to 40 cm H2O (p is less than 0.004) and greater than or equal to 50 cm H2O (p is less than 0.002). The incidence of alveolar rupture during postive pressure ventilation fell from 51 to 24% (p is less than 0.015) and bronchopulmonary dysplasia from 41 to 13% (p is less than 0.003). In addition, there was a decrease in the duration of mechanical ventilation (p is less than 0.02) and exposure to an FIO2 is greater than or equal to 0.6 (p = 0.07). The results confirm the intimate relationship of pulmonary barotrauma, as reflected by the occurrence of alveolar rupture during positive pressure inflation of the lungs, to the subsequent development of bronchopulmonary dysplasia and that prevention of the former is associated with a concomitant fall in incidence of the latter.

Follow-Up Studies↗
PubMed1978

Amelioration of bronchopulmonary dysplasia after vitamin E administration. A preliminary report.

We studied the effect of vitamin E on the development of bronchopulmonary dysplasis in neonates with respiratory-distress syndrome. Twenty infants received vitamin E administered intramuscularly during the acute phase of the syndrome, and 20 infants served as controls. Administration of vitamin E significantly increased the serum vitamin E concentration. Nine vitamin-treated and 13 control patients required supplemental oxygen for longer than 250 hours; all were treated with positive-pressure ventilation and endotracheal continuous distending airway pressure. Six of those 13 controls had x-ray changes consistent with bronchopulmonary dysplasia, and four died. None of the nine vitamin-treated patients had changes characteristic of bronchopulmonary dysplasia (P = 0.046), and all survived. Administration of vitamin E during the acute phase of the respiratory-distress syndrome appears to modify the development of bronchopulmonary dysplasis.

Bronchial Diseases↗
PubMed1979

Morphologic aspects of bronchopulmonary dysplasia.

Some of the morphologic changes of bronchopulmonary dysplasia are frequently found in infants dying of the infantile respiratory distress syndrome, so the frequency of BPD is more frequent as determined morphologically than as determined clinically. Morphologic differences have been described between the lesions of oxygen poisoning and those of BPD, but there are probably no true qualitative differences and such differences as exist are quantitative ones. Clinical and functional studies suggest that lung damage in infancy and early childhood may result in residual functional abnormalities in older childhood, and to a predisposition to chronic airflow obstruction in later life. It is hypothesized that this may be brought about by alteration in postnatal lung growth. Two patients who had an operation for diaphragmatic hernia on the first day of life and who died 8 and 64 months later were used to illustrate this point, since both had obviously abnormal lung structure at the time of death.

Adult↗
PubMed2026

Umbilical Cord-Derived Cell-Based Interventions for Bronchopulmonary Dysplasia and Related Complications in Preterm Infants: A Bayesian Sparse-Data Meta-Analysis.

Bronchopulmonary dysplasia (BPD) is a major complication of prematurity with limited disease-modifying therapies. We evaluated umbilical cord-derived cell-based interventions for BPD and related complications in preterm infants. This Preferred Reporting Items for Systematic Reviews and Meta-Analyses 2020-based systematic review and meta-analysis were registered in PROSPERO. PubMed, Cochrane Library, Web of Science, CNKI, and Wanfang were searched from inception to June 14, 2026. Comparative clinical studies of umbilical cord-derived cell-based interventions in preterm infants at risk of or diagnosed with BPD were included. Outcomes included BPD, BPD severity, death, persistent pulmonary hypertension of the newborn (PPHN), patent ductus arteriosus (PDA), intraventricular hemorrhage (IVH), necrotizing enterocolitis (NEC), retinopathy of prematurity (ROP), late-onset sepsis (LOS), and adverse events (AEs). Bayesian random-effects meta-analysis used a binomial-normal hierarchical model to estimate pooled odds ratios (ORs), 95% credible intervals (CrIs), prediction intervals, and heterogeneity. Twelve studies were included. Umbilical cord-derived cell-based interventions showed a possible protective effect on overall BPD (OR, 0.48; 95% CrI, 0.14-1.20). Stronger associations were observed for severe BPD (OR, 0.17; 95% CrI, 0.01-0.85), moderate or severe BPD (OR, 0.28; 95% CrI, 0.09-0.70), and ROP stage ≥3 (OR, 0.17; 95% CrI, 0.02-0.65). No conclusive benefit or harm was observed for death, PPHN, PDA, IVH, NEC, or LOS. No treatment-related serious AEs were identified. However, prediction intervals were generally wide, and the certainty of evidence was low to very low for most outcomes. Umbilical cord-derived cell-based interventions may reduce the risk of moderate or severe BPD in preterm infants, with an additional potential benefit for ROP stage ≥3. Current evidence remains limited, and larger randomized trials with standardized outcomes and long-term follow-up are needed.

Humans↗
PubMed1976

Asymmetric lung involvement in bronchopulmonary dysplasia.

The radiographic distribution of pulmonary abnormalities in bronchopulmonary dysplasia (BPD) in all previously reported cases has been bilateral and generalized. The authors studied 11 premature infants who had BPD that was primarily unilateral. The striking feature in each of these patients was the occurrence of an episode of prolonged unilateral atelectasis or tension pneumathorax. Few, if any, radiographic manifestations of BPD developed. Results of a detailed analysis of oxygen exposure and respirator therapy during the periods of unequal lung ventilation further characterizes the protective effect of atelectasis and tension pneumothorax in the development of BPD.

Female↗
PubMed1977

Bronchopulmonary dysplasia in premature infants. A radiological and pathological correlation.

In a group of 70 premature and newborn infants, treated with artificial ventilation, 24.3% developed bronchopulmonary dysplasia (BPD). Only in a very few cases did the typical radiological stages, as described by Northway, succeed each other in a chronological order. It is impossible to differentiate BPD stage I or II from RDS stage III and IV without a knowledge of the clinical course and of the duration of artificial ventilation. The lower the gestational age, the more severe and earlier do the radiological and histological changes occur. The radiological differential diagnosis of BPD includes Wilson-Mikity-syndrome, congenital pulmonary lymphangiectasia, neonatal tuberculosis, cystic fibrosis and Hamman-Rich-syndrome.

Bronchial Diseases↗
PubMed1977

Twelve years' experience with bronchopulmonary dysplasia.

A retrospective study of 299 successive infants who were ventilated for respiratory distress syndrome (RDS) showed that 62 (21%) developed radiographic stage VI bronchopulmonary dysplasia (BPD). The largest, most mature, and least ill infants tended to survive without developing BPD; the smallest, least mature, and most ill infants tended to die without developing BPD. The patients who developed BPD tended to be intermediate in terms of weight, maturity, and severity of disease; they required longer exposures to elevated oxygen and assisted ventilation than patients who did not develop BPD. The data suggest that in addition to varying individual susceptibility (primarily degree of immaturity and initial severity of disease), elevated oxygen is more important than mechanical ventilation in the pathogenesis of BPD.

Child↗
PubMed1979

Preferential distribution of lobar emphysema and atelectasis in bronchopulmonary dysplasia.

The chest roentgenograms of 142 neonates who survived mechanical ventilation for respiratory distress syndrome (N = 99) and prolonged apnea (N = 43) were reviewed. Thirty-seven infants had bronchopulmonary dysplasia (BPD) and 17 of these developed lobar hyperinflation of the right lower lobe and collapse of the right upper lobe. Regional lung function was measured with a xenon 133 technique in three of these infants and in five other patients who either died or were lost to follow-up. All had BPD with right lower lobe overinflation. Ventilation was less in the lower regions than the upper regions bilaterally (P less than .001), indicating that the hyperinflation of the lower lobes was not compensatory for upper lobe collapse but was due to emphysema. Mean regional perfusion was equal in the upper and lower regions of the chest. This preferential distribution of lobaremphysema and ipsilateral atelectasis in BPD tended to present and regress simultaneously, but in many infants it lasted as long as eight weeks. Only one infant with persistent atelectasis developed pneumonia. The best mode of therapy appears to be supportive.

Apnea↗
PubMed1976

Pathogenesis of bronchopulmonary dysplasia following hyaline membrane disease.

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 with HMD showed that: a) From the fourth or fifth day, the surface tension of lung extracts fell, inclusion bodies became more plentiful, and air saccules with patent airways could be inflated with air, even when severe changes due to BPD were present. b) There was a highly statistically significant correlation between the most serious lesions of BPD--damage to airways followed by excessive repair and fibrosis--and the use of high (greater than 35 cm H2O) peak airway pressures during mechanical ventilation in life. c) Damage due to oxygen breathing could not be reliably identified although some of the lesions, particularly edema and fibroplasia in intersaccular septa, may have been caused by oxygen. d) Evidence of pulmonary hypertension was present in infants surviving for more than a month with severe lung damage, and the ductus arteriosus was always open. We conclude that the most important factor in the pathogenesis of BPD following HMD is mechanical trauma to the lung from the use of excessively high peak airway pressures during mechanical ventilation.

Bronchial Diseases↗
PubMed1979

The immature monkey as a model for studies of bronchopulmonary dysplasia.

The monkey is a potential model for BPD since there is considerable background information on the normal-developing lung, the prematurely delivered infant is viable, HMD can be produced, the infant is large enough to permit physiologic measurements, and it should be possible to test the effects of positive pressure, oxygen, and pharmacologic agents. Clearly further information is needed on the cellular and subcellular changes occurring during the acute and recovery stages of HMD. The monkey has already proven to be of value in this inquiry. Studies on mechanisms of altered lung repair by various injurious agents are needed, and will require an animal model as well as in vitro systems. Basic understanding of the pathogenesis of bronchopulmonary dysplasia with establishment of the relative importance of the contributing factors should help in our efforts to prevent or minimize chronic lung disease in the newborn infant.

Animals↗
PubMed1978

Unchanged incidence of bronchopulmonary dysplasia in survivors of hyaline membrane disease.

To test the hypothesis that decreased mortality from severe HMD will result in increased morbidity from BPD, chest films of 30-day survivors of severe HMD were reviewed for evidence of Northway's Stage IV BPD. During July, 1970 to June, 1971, 20 survivors of severe HMD were identified; one case of Stage IV BPD was found in this group. During July 1974-June 1975, 80 survivors of severe HMD were identified; five infants had BPD. In spite of more survivors of severe HMD, no increase in the incidence of BPD could be demonstrated.

Bronchial Diseases↗