ArticleNeonatology2014
Repeated β2-adrenergic receptor agonist therapy attenuates the response to rescue bronchodilation in a hyperoxic newborn mouse model.
Article in Neonatology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Hydrogen sulfide alleviates hyperoxia effects on mitochondria in human developing airway smooth muscle.JCI insight · 2026Article
- S-nitrosylation of pVHL regulates βProceedings of the National Academy of Sciences of the United States of America · 2025Article
- The CD146-HIF-1α axis regulates epithelial cell migration and alveolar maturation in a mouse model of bronchopulmonary dysplasia.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- Response to first dose of inhaled albuterol in mechanically ventilated preterm infants.Journal of perinatology : official journal of the California Perinatal Association · 2021Article
- Airway relaxation mechanisms and structural basis of osthole for improving lung function in asthma.Science signaling · 2020Article
- Pathophysiology of SARS-CoV-2 in Lung of Diabetic Patients.Frontiers in physiology · 2020Review
- Tracheomalacia in bronchopulmonary dysplasia: Trachealis hyper-relaxant responses to S-nitrosoglutathione in a hyperoxic murine model.Pediatric pulmonology · 2019Article
- Rodent models of respiratory control and respiratory system development-Clinical significance.Respiratory physiology & neurobiology · 2019Review
- Effects of salbutamol and phlorizin on acute pulmonary inflammation and disease severity in experimental sepsis.PloS one · 2019Article
- A NovelJournal of infectious pulmonary diseases · 2017Article
- S-Nitrosoglutathione Attenuates Airway Hyperresponsiveness in Murine Bronchopulmonary Dysplasia.Molecular pharmacology · 2016Article
- Animal models of bronchopulmonary dysplasia. The term mouse models.American journal of physiology. Lung cellular and molecular physiology · 2014Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundPreterm infants with neonatal lung injury are prone to wheezing and are often treated with β2-adrenergic receptor (β-AR) agonists although the benefits of β-AR agonists may be lost with chronic use.
objectiveTo investigate if repeated β-AR agonist exposure downregulates β-ARs in the immature lung resulting in a decreased response to bronchodilator rescue and whether hyperoxic exposure aggravates this response.
methodsNewborn mice were raised for 21 days in 60 or 21% oxygen and received daily aerosols of formoterol or saline. Respiratory system resistance (Rrs) and compliance (Crs) were measured in response to methacholine challenge and rescue bronchodilation with levalbuterol. Western blot analysis quantified the relative amount of lung β-ARs.
resultsHyperoxia increased the airway reactivity to methacholine. Animals raised in hyperoxia that received daily formoterol were most sensitive to methacholine and exhibited a blunted response to levalbuterol bronchodilation. Hyperoxia-exposed animals receiving daily formoterol versus saline showed a significant decrease in the relative amount of lung β-ARs.
conclusionsIn this hyperoxia-exposed neonatal mouse model, repeated β-AR agonist treatments increased the airway reactivity and attenuated the response to a rescue bronchodilator. The blunted bronchodilator response could be explained by a reduced quantity of lung β-ARs. Our findings may account for the time-dependent decrease in the therapeutic benefit of β-AR agonists in preterm infants with neonatal lung injury, which may have clinical consequences for patients already prone to airway hyperreactivity.
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