Evidence map›Paper›PMID 22331413›Full record

ArticleThe Journal of physiology2012

A role for xanthine oxidase in the control of fetal cardiovascular function in late gestation sheep.

E A Herrera, A D Kane, J A Hansell, A S Thakor, B J Allison, Y Niu, D A Giussani

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2012. 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
3.3field-weighted citation impact, top 8% 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, 38 citations in OpenAlex.

  1. Antioxidants: powering the fight against fetal hypoxia.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Review
  2. Article
  3. Pathomechanisms of Prenatally Programmed Adult Diseases.Antioxidants (Basel, Switzerland) · 2023
    Review
  4. Article
  5. Preeclampsia link to gestational hypoxia.Journal of developmental origins of health and disease · 2019
    Review
  6. Article
  7. Mechanisms of death in structurally normal stillbirths.Journal of perinatal medicine · 2019
    Observational
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

E A HerreraDepartment of Physiology Development & Neuroscience, University of Cambridge, Cambridge CB2 3EG, UK.
A D Kane
J A Hansell
A S Thakor
B J Allison
Y Niu
D A Giussani
University of Cambridge · GB

Funding

Biotechnology and Biological Sciences Research CouncilBritish Heart Foundation RG/06/006/22028
6 · The paper itself

Abstract

Virtually nothing is known about the effects on fetal physiology of xanthine oxidase inhibition. This is despite maternal treatment with the xanthine oxidase inhibitor allopurinol being considered in human complicated pregnancy to protect the infant’s brain from excessive generation of ROS.We investigated the in vivo effects of maternal treatment with allopurinol on fetal cardiovascular function in ovine pregnancy in late gestation. Under anaesthesia, pregnant ewes and their singleton fetus were instrumented with vascular catheters and flow probes around an umbilical and a fetal femoral artery at 118±1 dGA (days of gestational age; termca. 145 days). Five days later, mothers were infused I.V. with either vehicle (n =11) or allopurinol (n =10). Fetal cardiovascular function was stimulated with increasing bolus doses of phenylephrine (PE) following maternal vehicle or allopurinol. The effects of maternal allopurinol on maternal and fetal cardiovascular function were also investigated following fetal NO blockade (n =6) or fetal β1-adrenergic antagonism (n =7). Maternal allopurinol led to significant increases in fetal heart rate, umbilical blood flow and umbilical vascular conductance, effects abolished by fetal β1-adrenergic antagonism but not by fetal NO blockade. Maternal allopurinol impaired fetal α1-adrenergic pressor and femoral vasopressor responses and enhanced the gain of the fetal cardiac baroreflex. These effects of maternal allopurinol were restored to control levels during fetal NO blockade. Maternal treatment with allopurinol induced maternal hypotension, tachycardia and acid–base disturbance. We conclude that maternal treatment with allopurinol alters in vivo maternal, umbilical and fetal vascular function via mechanisms involving NO and β1-adrenergic stimulation. The evidence suggests that the use of allopurinol in clinical practice should be approached with caution.

Indexed as

Adrenergic beta-1 Receptor AntagonistsAllopurinolAnimalsCardiovascular Physiological PhenomenaCardiovascular SystemFemaleFetusGestational AgeHeart Rate, FetalNitric OxidePregnancyPregnancy ComplicationsRegional Blood FlowSheepUric AcidXanthine OxidaseAdrenergic beta-1 Receptor AntagonistsAllopurinolNitric OxideUric AcidXanthine Oxidase

Identifiers

PMID22331413
PMCPMC3573306
OpenAlexW2106901294

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.