Evidence map›Paper›PMID 12562957›Full record

ArticleThe Journal of physiology2003

Prenatal dexamethasone leads to both endothelial dysfunction and vasodilatory compensation in sheep.

Judit Molnar, David C Howe, Mark J M Nijland, Peter W Nathanielsz

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
10.2field-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

21 citing papers in PubMed, 63 citations in OpenAlex.

  1. Review
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  4. Poor perinatal growth impairs baboon aortic windkessel function.Journal of developmental origins of health and disease · 2018
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  8. Review
  9. Antenatal betamethasone has a sex-dependent effect on the in vivo response to endothelin in adult sheep.American journal of physiology. Regulatory, integrative and comparative physiology · 2013
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  18. Newborn lamb coronary artery reactivity is programmed by early gestation dexamethasone before the onset of systemic hypertension.American journal of physiology. Regulatory, integrative and comparative physiology · 2005
    Article
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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.

Judit MolnarEdward Melby Cardiovascular Research Laboratory, Department of Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14850, USA.
David C Howe
Mark J M Nijland
Peter W Nathanielsz
Cornell University · US

Funding

PARTURITION AND FETAL PRIMATE HYPOTHALAMIC FUNCTIONP01HD021350 · NICHD · UNIVERSITY OF WYOMING · PI NATHANIELSZ, PETER W. · 1987 to 2018
$19.9M
Glucocorticoid Programming of the Peripheral VasculatureR01HL068649 · NHLBI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI NATHANIELSZ, PETER W. · 2004 to 2007
$1.5M
TRH AND GLUCOCORTICOID ACTIONS ON THE FETAL LUNGR01HL055416 · NHLBI · CORNELL UNIVERSITY ITHACA · PI NATHANIELSZ, PETER W · 1997 to 2000
$311k
NHLBI NIH HHS HL21350NHLBI NIH HHS HL55416NHLBI NIH HHS R01 HL068649NICHD NIH HHS P01 HD021350
6 · The paper itself

Abstract

We investigated long-term cardiovascular effects in the offspring of sheep exposed to prenatal dexamethasone (DM). We assessed in vitro vascular responsiveness and evaluated endothelial nitric oxide synthase (eNOS) message and protein levels in femoral muscle removed from 5-month-old sheep. Dexamethasone was administered i.m. to pregnant ewes as 3 weekly courses (4 x 2 mg at 12 h intervals), starting on day 103 of gestation (term approximately 149 days). Ewes were allowed to lamb. At 5 months of age a carotid catheter was placed for blood pressure measurement and hamstring muscle was removed from the lambs under general anaesthesia. We demonstrate that following prenatal DM exposure in the 5-month-old offspring: (1) blood pressure is unchanged; (2) as previously reported in the fetus, sensitivity to endothelin-1 (ET) is increased; (3) acetylcholine-induced relaxation is increased; (4) L-NAME suppressible vasodilatory response to ET is abolished; (5) there is no change in endothelium-independent vasodilatation; and (6) there is no change in eNOS RNA and protein levels, when compared to saline treated controls. We speculate that decreased agonist-induced NO release is not due to alteration in gene expression, but is more likely to be a post-transcriptional event. In summary, the lack of a difference in resting mean arterial pressure (MAP) between DM and control lambs indicates that the compensation we have previously demonstrated in the fetus following glucocorticoid exposure persists to 5 months postnatal age. Compensation is likely due to non-NO-dependent mechanisms, since no evidence was found of upregulated NOS.

Indexed as

Prenatal Exposure Delayed EffectsAnimalsBlood PressureDexamethasoneEndothelium, VascularEnzyme InhibitorsFemaleGene Expression Regulation, EnzymologicGlucocorticoidsMicrocirculationNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide SynthaseNitric Oxide Synthase Type IIIPregnancyReverse Transcriptase Polymerase Chain ReactionDexamethasoneEnzyme InhibitorsGlucocorticoidsNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide SynthaseNitric Oxide Synthase Type III

Identifiers

PMID12562957
PMCPMC2342609
OpenAlexW2170874195

What Socratic 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 Socratic graph.