Evidence map›Paper›PMID 15760943›Full record

ReviewThe Journal of physiology2005

The effects of anaemia as a programming agent in the fetal heart.

L Davis, K L Thornburg, G D Giraud

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
6.1field-weighted citation impact, top 4% 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

15 citing papers in PubMed, 41 citations in OpenAlex.

  1. Observational
  2. Article
  3. Fetal brain sparing in a mouse model of chronic maternal hypoxia.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019
    Article
  4. Article
  5. Chronic hypoxia alters maternal uterine and fetal hemodynamics in the full-term pregnant guinea pig.American journal of physiology. Regulatory, integrative and comparative physiology · 2017
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. The programming of cardiovascular disease.Journal of developmental origins of health and disease · 2015
    Review
  11. How to build a healthy heart from scratch.Advances in experimental medicine and biology · 2014
    Review
  12. Review
  13. Article
  14. Article
  15. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 2 countries.

L DavisDepartment of Obstetrics and Gynecology, Oregon Health Sciences University, Portland, OR 97201-3098, USA. davislo@ohsu.edu
K L Thornburg
G D Giraud
Oregon Health & Science University · USPortland VA Medical Center · US

Funding

ULTRASOUND IMAGING COREP01HD034430 · NICHD · OREGON HEALTH & SCIENCE UNIVERSITY · PI THOMAS, GEORGE VICTOR · 1997 to 2017
$20.7M
WATER COMPARTMENTALIZATION IN CHRONIC FETAL ANEMIAR01HL045043 · NHLBI · OREGON HEALTH & SCIENCE UNIVERSITY · PI DAVIS, LOWELL E · 1996 to 2007
$1.9M
WATER COMPARTMENTALIZATION IN FETAL ANEMIAR29HL045043 · NHLBI · OREGON HEALTH AND SCIENCE UNIVERSITY · PI DAVIS, LOWELL E · 1992 to 1995
–
NHLBI NIH HHS HL45043NHLBI NIH HHS R01 HL045043NICHD NIH HHS P01 HD034430NICHD NIH HHS P01HD34430
6 · The paper itself

Abstract

The intrauterine environment plays a powerful role in determining the life-long risk of cardiovascular disease. A number of stressors are well known to affect the development of the cardiovascular system in utero including over/under maternal nutrition, excess glucocorticoid and chronic hypoxia. Chronic fetal anaemia in sheep is a complex stressor that alters cardiac loading conditions, causes hypoxic stress and stimulates large changes in flow to specific tissues, including large increases in resting coronary blood flow and conductance. Decreased viscosity can account for approximately half of the increased flow. It appears that immature hearts are 'plastic' in that increases in coronary conductance with fetal anaemia persist into adulthood even if the anaemia is corrected before birth. These large changes in conductance are possible only through extensive remodelling of the coronary tree. Adult hearts that were once anaemic in utero are more resistant to hypoxic stress as adults but it is not known whether such an adaptation would be deleterious in later life. These studies indicate the need for investigation into the basic mechanisms of coronary tree remodelling in the immature myocardium. New information on these mechanisms is likely to lead to better prevention of and therapies for adult-onset coronary disease.

Indexed as

Coronary CirculationAnemia, NeonatalAnimalsAnimals, NewbornFemaleFetal HeartFetal HypoxiaHumansInfant, NewbornPregnancySheep

Identifiers

PMID15760943
PMCPMC1464492
OpenAlexW2150674341

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.