Evidence map›Paper›PMID 22640932›Full record

ReviewRespiratory physiology & neurobiology2013

Chronic hyperoxia and the development of the carotid body.

Ryan W Bavis, Sarah C Fallon, Elizabeth F Dmitrieff

Open access · greenAbstract readReview
In one paragraph

Review in Respiratory physiology & neurobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.9field-weighted citation impact, top 16% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Article
  3. Structural Plasticity of the Carotid Body.Advances in anatomy, embryology, and cell biology · 2023
    Article
  4. Apnea of prematurity and sudden infant death syndrome.Handbook of clinical neurology · 2022
    Review
  5. Review
  6. Perinatal Hypoxemia and Oxygen Sensing.Comprehensive Physiology · 2021
    Article
  7. Experimental Evidence of AFrontiers in physiology · 2021
    Article
  8. Article
  9. Review
  10. Review
  11. Acute and chronic changes in the control of breathing in a rat model of bronchopulmonary dysplasia.American journal of physiology. Lung cellular and molecular physiology · 2019
    Article
  12. Article
  13. Cardioventilatory Control in Preterm-born Children and the Risk of Obstructive Sleep Apnea.American journal of respiratory and critical care medicine · 2018
    Article
  14. Article
  15. Article
  16. Article
  17. Challenges and opportunities in developmental integrative physiology.Comparative biochemistry and physiology. Part A, Molecular & integrative physiology · 2015
    Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Ryan W BavisDepartment of Biology, Bates College, Lewiston, ME 04240, USA. rbavis@bates.edu
Sarah C Fallon
Elizabeth F Dmitrieff
Bates College · US

Funding

The Maine Biomedical Research Network (INBRE)P20GM103423 · NIGMS · MOUNT DESERT ISLAND BIOLOGICAL LAB · PI Dustin Lynn Updike · 2012 to 2026
$60.0M
WNT SIGNALING IN THE DEVELOPING GASTROINTESTINAL TRACTP20RR016463 · NCRR · MOUNT DESERT ISLAND BIOLOGICAL LAB · PI HAND, PATRICIA H. · 2001 to 2011
$41.0M
NCRR NIH HHS P20 RR016463NCRR NIH HHS P20 RR-016463-12NIGMS NIH HHS P20 GM-103423NIGMS NIH HHS P20 GM103423
6 · The paper itself

Abstract

Preterm infants often experience hyperoxia while receiving supplemental oxygen. Prolonged exposure to hyperoxia during development is associated with pathologies such as bronchopulmonary dysplasia and retinopathy of prematurity. Over the last 25 years, however, experiments with animal models have revealed that moderate exposures to hyperoxia (e.g., 30-60% O(2) for days to weeks) can also have profound effects on the developing respiratory control system that may lead to hypoventilation and diminished responses to acute hypoxia. This plasticity, which is generally inducible only during critical periods of development, has a complex time course that includes both transient and permanent respiratory deficits. Although the molecular mechanisms of hyperoxia-induced plasticity are only beginning to be elucidated, it is clear that many of the respiratory effects are linked to abnormal morphological and functional development of the carotid body, the principal site of arterial O(2) chemoreception for respiratory control. Specifically, developmental hyperoxia reduces carotid body size, decreases the number of chemoafferent neurons, and (at least transiently) diminishes the O(2) sensitivity of individual carotid body glomus cells. Recent evidence suggests that hyperoxia may also directly or indirectly impact development of the central neural control of breathing. Collectively, these findings emphasize the vulnerability of the developing respiratory control system to environmental perturbations.

Indexed as

AnimalsCarotid BodyHumansHyperoxia

Identifiers

PMID22640932
PMCPMC3448014
OpenAlexW1993262488

What Socratic holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.