Evidence map›Paper›PMID 22106179›Full record

ArticleThe Journal of physiology2012

Statin treatment depresses the fetal defence to acute hypoxia via increasing nitric oxide bioavailability.

Andrew D Kane, Emilio A Herrera, Jeremy A Hansell, Dino A Giussani

Open access · bronzeAbstract 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 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
10.8field-weighted citation impact, top 1% 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

25 citing papers in PubMed, 70 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. Review
  4. Article
  5. Article
  6. The role of gasotransmitters in neonatal physiology.Nitric oxide : biology and chemistry · 2020
    Review
  7. Article
  8. Article
  9. Article
  10. Pravastatin ameliorates placental vascular defects, fetal growth, and cardiac function in a model of glucocorticoid excess.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  11. Divergence of mechanistic pathways mediating cardiovascular aging and developmental programming of cardiovascular disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016
    Article
  12. Article
  13. Pravastatin to prevent recurrent fetal death in massive perivillous fibrin deposition of the placenta (MPFD).The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians · 2016
    Article
  14. Review
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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

4 authors at 1 institution in 1 country.

Andrew D KaneDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge CB2 3EG, UK.
Emilio A Herrera
Jeremy A Hansell
Dino A Giussani
University of Cambridge · GB

Funding

British Heart Foundation RG/06/006/22028
6 · The paper itself

Abstract

In addition to lowering cholesterol, statins increase nitric oxide (NO) bioavailability, improving endothelial function. In the fetus, enhanced NO during acute hypoxia opposes the fetal peripheral vasoconstrictor response, part of the brain-sparing defence. This study tested the hypothesis that treatment with statins depresses the fetal circulatory response to acute hypoxic stress via increasing NO bioavailability. Under anaesthesia, 12 fetal sheep at 118 ± 1 days of gestation (term ca 145 days) were instrumented with vascular catheters and a femoral artery Transonic flow probe for chronic recording. Five days later, all animals were subjected to 30 min of acute hypoxia (fetal arterial partial pressure of O(2) ( ) reduced by ca 50%) before and 24 h after fetal treatment with pravastatin (25 mg i.v.). In half of the fetuses (n = 6), responses to hypoxia post-pravastatin were evaluated during NO synthesis blockade. Fetal exposure to pravastatin did not affect fetal basal cardiovascular function. Fetal was similarly reduced in all acute hypoxia experiments from ca 21 to 10 mmHg. Fetal exposure to pravastatin markedly diminished the fetal femoral vasoconstrictor (5.1 ± 0.9 vs. 2.5 ± 0.5 mmHg (ml min(-1))(-1)) and lactic acidaemic (4.4 ± 0.5 vs. 3.0 ± 0.3 mm) responses to acute hypoxia (both P < 0.05), without affecting plasma catecholamine responses. Post-pravastatin, the circulatory (5.8 ± 1.5 mmHg (ml min(-1))(-1)) and metabolic (3.9 ± 0.3 mm) responses could be restored to control levels during fetal treatment with NO synthase blockade. Pravastatin depresses the fetal cardiovascular and metabolic defences to acute hypoxia via increasing NO bioavailability. The use of statins during pregnancy should be viewed with extreme caution.

Indexed as

AnimalsAnticholesteremic AgentsBiological AvailabilityBlood Gas AnalysisCardiovascular SystemCatecholaminesEndocrine SystemFemaleFetusHypoxiaModels, AnimalNitric OxideNitric Oxide SynthasePravastatinPregnancySheepAnticholesteremic AgentsCatecholaminesNitric OxideNitric Oxide SynthasePravastatin

Identifiers

PMID22106179
PMCPMC3285068
OpenAlexW1823662212

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.