Evidence map›Paper›PMID 27007694›Full record

ArticlePloS one2016

The Early Endocrine Stress Response in Experimental Subarachnoid Hemorrhage.

Christoffer Nyberg, Torbjörn Karlsson, Lars Hillered, Mats Stridsberg, Elisabeth Ronne Engström

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 33% 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

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Trial
  2. Article
  3. Observational
  4. Review
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

5 authors at 1 institution in 1 country.

Christoffer NybergDepartment of Neuroscience, Section of Neurosurgery, Uppsala University, Uppsala, Sweden.
Torbjörn KarlssonDepartment of Surgical Sciences, Section of Anesthesiology and Intensive care, Uppsala University, Uppsala, Sweden.
Lars HilleredDepartment of Neuroscience, Section of Neurosurgery, Uppsala University, Uppsala, Sweden.
Mats StridsbergDepartment of Medical Sciences, Uppsala University, Uppsala, Sweden.
Elisabeth Ronne EngströmDepartment of Neuroscience, Section of Neurosurgery, Uppsala University, Uppsala, Sweden.
Uppsala University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionIn patients with severe illness, such as aneurysmal subarachnoid hemorrhage (SAH), a physiologic stress response is triggered. This includes activation of the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system. The aim of this study was to investigate the very early responses of these systems.

methodsA porcine animal model of aneurysmal SAH was used. In this model, blood is injected slowly to the basal cisterns above the anterior skull base until the cerebral perfusion pressure is 0 mm Hg. Sampling was done from blood and urine at -10, +15, +75 and +135 minutes from time of induction of SAH. Analyses of adrenocorticotropic hormone (ACTH), cortisol, aldosterone, catecholamines and chromogranin-A were performed.

resultsPlasma ACTH, serum cortisol and plasma aldosterone increased in the samples following induction of SAH, and started to decline after 75 minutes. Urine cortisol also increased after SAH. Urine catecholamines and their metabolites were found to increase after SAH. Many samples were however below detection level, not allowing for statistical analysis. Plasma chromogranin-A peaked at 15 minutes after SAH, and thereafter decreased.

conclusionsThe endocrine stress response after aneurysmal SAH was found to start within 15 minutes in the HPA axis with early peak values of ACTH, cortisol and aldosterone. The fact that the concentrations of the HPA axis hormones decreased 135 minutes after SAH may suggest that a similar pattern exists in SAH patients, thus making it difficult to catch these early peak values. There were also indications of early activation of the sympathetic nervous system, but the small number of valid samples made interpretation difficult.

Indexed as

Disease Models, AnimalHypothalamo-Hypophyseal SystemPituitary-Adrenal SystemStress, PhysiologicalAdrenocorticotropic HormoneAldosteroneAnimalsCatecholaminesFemaleHydrocortisoneMaleSubarachnoid HemorrhageSwineAdrenocorticotropic HormoneAldosteroneCatecholaminesHydrocortisone

Identifiers

PMID27007694
PMCPMC4805209
OpenAlexW2306595835

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.