Evidence map›Paper›PMID 24247986›Full record

ArticleThe Journal of physiology2014

Xanthine oxidase and the fetal cardiovascular defence to hypoxia in late gestation ovine pregnancy.

Andrew D Kane, Jeremy A Hansell, Emilio A Herrera, Beth J Allison, Youguo Niu, Kirsty L Brain, Joepe J Kaandorp, Jan B Derks, Dino A Giussani

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
9.8field-weighted citation impact, top 2% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Creatine for women in pregnancy for neuroprotection of the fetus.The Cochrane database of systematic reviews · 2014
    Pooled it
  2. Review
  3. Antioxidants: powering the fight against fetal hypoxia.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Mitochondria antioxidant protection against cardiovascular dysfunction programmed by early-onset gestational hypoxia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  11. Article
  12. Review
  13. The role of gasotransmitters in neonatal physiology.Nitric oxide : biology and chemistry · 2020
    Review
  14. Article
  15. Mechanisms of death in structurally normal stillbirths.Journal of perinatal medicine · 2019
    Observational
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 4 countries.

Andrew D KaneDepartment of Physiology, Development & Neuroscience, University of Cambridge, Cambridge CB2 3EG, UK. dag26@cam.ac.uk.
Jeremy A Hansell
Emilio A Herrera
Beth J Allison
Youguo Niu
Kirsty L Brain
Joepe J Kaandorp
Jan B Derks
Dino A Giussani
University of Cambridge · GBUtrecht University · NLInstituto de Neurociencia Biomédica · CL

Funding

Biotechnology and Biological Sciences Research Council BB/E002668/1British Heart Foundation RG/11/16/29260
6 · The paper itself

Abstract

Hypoxia is a common challenge to the fetus, promoting a physiological defence to redistribute blood flow towards the brain and away from peripheral circulations. During acute hypoxia, reactive oxygen species (ROS) interact with nitric oxide (NO) to provide an oxidant tone. This contributes to the mechanisms redistributing the fetal cardiac output, although the source of ROS is unknown. Here, we investigated whether ROS derived from xanthine oxidase (XO) contribute to the fetal peripheral vasoconstrictor response to hypoxia via interaction with NO-dependent mechanisms. Pregnant ewes and their fetuses were surgically prepared for long-term recording at 118 days of gestation (term approximately 145 days). After 5 days of recovery, mothers were infused i.v. for 30 min with either vehicle (n = 11), low dose (30 mg kg(-1), n = 5) or high dose (150 mg kg(-1), n = 9) allopurinol, or high dose allopurinol with fetal NO blockade (n = 6). Following allopurinol treatment, fetal hypoxia was induced by reducing maternal inspired O2 such that fetal basal P aO 2 decreased approximately by 50% for 30 min. Allopurinol inhibited the increase in fetal plasma uric acid and suppressed the fetal femoral vasoconstrictor, glycaemic and lactate acidaemic responses during hypoxia (all P < 0.05), effects that were restored to control levels with fetal NO blockade. The data provide evidence for the activation of fetal XO in vivo during hypoxia and for XO-derived ROS in contributing to the fetal peripheral vasoconstriction, part of the fetal defence to hypoxia. The data are of significance to the understanding of the physiological control of the fetal cardiovascular system during hypoxic stress. The findings are also of clinical relevance in the context of obstetric trials in which allopurinol is being administered to pregnant women when the fetus shows signs of hypoxic distress.

Indexed as

Blood PressureHeart RateAllopurinolAnimalsBlood GlucoseEnzyme InhibitorsFemaleFetal HeartFetal HypoxiaGestational AgeLactic AcidNitric OxideOxygenOxygen ConsumptionPregnancyReactive Oxygen SpeciesAllopurinolBlood GlucoseEnzyme InhibitorsLactic AcidNitric OxideOxygenReactive Oxygen SpeciesUric AcidXanthine Oxidase

Identifiers

PMID24247986
PMCPMC3930434
OpenAlexW1743581095

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.