Evidence map›Paper›PMID 18703410›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2008

Development of the ACTH and corticosterone response to acute hypoxia in the neonatal rat.

Eric D Bruder, Jennifer K Taylor, Kimberli J Kamer, Hershel Raff

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2008. 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
2.5field-weighted citation impact, top 11% 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, 46 citations in OpenAlex.

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  14. Renin knockout rat: control of adrenal aldosterone and corticosterone synthesis in vitro and adrenal gene expression.American journal of physiology. Regulatory, integrative and comparative physiology · 2015
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  19. Effect of high-dose total body irradiation on ACTH, corticosterone, and catecholamines in the rat.Translational research : the journal of laboratory and clinical medicine · 2011
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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.

Eric D BruderEndocrinology, St. Luke's Physician's Office Bldg., 2801 W. KK River Pky, Suite 245, Milwaukee, WI 53215, USA.
Jennifer K Taylor
Kimberli J Kamer
Hershel Raff
Medical College of Wisconsin · US

Funding

PERINATAL HYPOXIA: ADRENOCORTICAL-METABOLIC ADAPTATIONSR01DK054685 · NIDDK · MEDICAL COLLEGE OF WISCONSIN · PI RAFF, HERSHEL · 1999 to 2006
$1.3M
NIDDK NIH HHS DK-54685
6 · The paper itself

Abstract

Acute episodes of severe hypoxia are among the most common stressors in neonates. An understanding of the development of the physiological response to acute hypoxia will help improve clinical interventions. The present study measured ACTH and corticosterone responses to acute, severe hypoxia (8% inspired O(2) for 4 h) in neonatal rats at postnatal days (PD) 2, 5, and 8. Expression of specific hypothalamic, anterior pituitary, and adrenocortical mRNAs was assessed by real-time PCR, and expression of specific proteins in isolated adrenal mitochondria from adrenal zona fascisulata/reticularis was assessed by immunoblot analyses. Oxygen saturation, heart rate, and body temperature were also measured. Exposure to 8% O(2) for as little as 1 h elicited an increase in plasma corticosterone in all age groups studied, with PD2 pups showing the greatest response ( approximately 3 times greater than PD8 pups). Interestingly, the ACTH response to hypoxia was absent in PD2 pups, while plasma ACTH nearly tripled in PD8 pups. Analysis of adrenal mRNA expression revealed a hypoxia-induced increase in Ldlr mRNA at PD2, while both Ldlr and Star mRNA were increased at PD8. Acute hypoxia decreased arterial O(2) saturation (SPo(2)) to approximately 80% and also decreased body temperature by 5-6 degrees C. The hypoxic thermal response may contribute to the ACTH and corticosterone response to decreases in oxygen. The present data describe a developmentally regulated, differential corticosterone response to acute hypoxia, shifting from ACTH independence in early life (PD2) to ACTH dependence less than 1 wk later (PD8).

Indexed as

Adrenal GlandsAdrenocorticotropic HormoneAnimalsAnimals, NewbornBody TemperatureCorticosteroneCRF Receptor, Type 1Gene Expression Regulation, DevelopmentalHeart RateHypothalamo-Hypophyseal SystemHypothalamusHypoxiaNeuropeptide YOxygenPhosphoproteinsPituitary-Adrenal SystemAdrenocorticotropic HormoneCorticosteroneCRF Receptor, Type 1Neuropeptide YOxygenPhosphoproteinsProto-Oncogene Proteins c-fosReceptors, Corticotropin-Releasing HormoneReceptors, GlucocorticoidReceptors, LDLRNA, MessengerSteroidogenic Acute Regulatory Protein

Identifiers

PMID18703410
PMCPMC2576086
OpenAlexW1977108909

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.