ArticleRespiratory physiology & neurobiology2012
Carotid body growth during chronic postnatal hyperoxia.
Article in Respiratory physiology & neurobiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Effect of Intermittent Hypoxemia and Hyperoxemia during the Neonatal Period on Control of Breathing Function among Infants Born Extremely Preterm.The Journal of pediatrics · 2025Observational
- Comparative exploration of the carotid body in domestic animals: morphology, physiology, histology, and pathology.Frontiers in veterinary science · 2024Review
- Blood and urine biomarkers associated with long-term respiratory dysfunction following neonatal hyperoxia exposure: Implications for prematurity and risk of SIDS.Respiratory physiology & neurobiology · 2020Article
- Combined effects of intermittent hyperoxia and intermittent hypercapnic hypoxia on respiratory control in neonatal rats.Respiratory physiology & neurobiology · 2019Article
- Ventilatory and chemoreceptor responses to hypercapnia in neonatal rats chronically exposed to moderate hyperoxia.Respiratory physiology & neurobiology · 2017Article
- Cardiorespiratory events in preterm infants: etiology and monitoring technologies.Journal of perinatology : official journal of the California Perinatal Association · 2016Review
- Chronic intermittent hyperoxia alters the development of the hypoxic ventilatory response in neonatal rats.Respiratory physiology & neurobiology · 2016Article
- Role of TrkB during the postnatal development of the rat carotid body.Respiratory physiology & neurobiology · 2015Article
- Challenges and opportunities in developmental integrative physiology.Comparative biochemistry and physiology. Part A, Molecular & integrative physiology · 2015Review
- Postnatal development of eupneic ventilation and metabolism in rats chronically exposed to moderate hyperoxia.Respiratory physiology & neurobiology · 2014Article
- Perinatal hyperoxia exposure impairs hypoxia-induced depolarization in rat carotid body glomus cells.Respiratory physiology & neurobiology · 2013Article
- Carotid chemoreceptor development in mice.Respiratory physiology & neurobiology · 2013Review
- Chronic hyperoxia and the development of the carotid body.Respiratory physiology & neurobiology · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Rats reared in hyperoxia have smaller carotid bodies as adults. To study the time course and mechanisms underlying these changes, rats were reared in 60% O(2) from birth and their carotid bodies were harvested at various postnatal ages (P0-P7, P14). The carotid bodies of hyperoxia-reared rats were smaller than those of age-matched controls beginning at P4. In contrast, 7d of 60% O(2) had no effect on carotid body size in rats exposed to hyperoxia as adults. Bromodeoxyuridine (BrdU) and TdT-mediated dUTP nick end labeling (TUNEL) were used to assess cell proliferation and DNA fragmentation at P2, P4, and P6. Hyperoxia reduced the proportion of glomus cells undergoing cell division at P4; although a similar trend was evident at P2, hyperoxia no longer affected cell proliferation by P6. The proportion of TUNEL-positive glomus cells was modestly increased by hyperoxia. We did not detect changes in mRNA expression for proapoptotic (Bax) or antiapoptotic (Bcl-X(L)) genes or transcription factors that regulate cell cycle checkpoints (p53 or p21), although mRNA levels for cyclin B1 and cyclin B2 were reduced. Collectively, these data indicate that hyperoxia primarily attenuates postnatal growth of the carotid body by inhibiting glomus cell proliferation during the first few days of exposure.
Indexed as
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What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.