Evidence map›Paper›PMID 24951620›Full record

ArticleThe Journal of physiology2014

Hypometabolism and hypothermia in the rat model of endotoxic shock: independence of circulatory hypoxia.

Joshua J Corrigan, Monique T Fonseca, Elizabeth A Flatow, Kevin Lewis, Alexandre A Steiner

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 12% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

  1. Pooled it
  2. The poikilothermic hypothesis of sepsis.Critical care (London, England) · 2026
    Review
  3. Article
  4. Metabolic profiling in experimental guinea pig models of bacterial and allergic inflammation.Metabolomics : Official journal of the Metabolomic Society · 2025
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Potential biomarkers in septic shock besides lactate.Experimental biology and medicine (Maywood, N.J.) · 2020
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
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 3 institutions in 2 countries.

Joshua J CorriganDepartment of Pharmaceutical Sciences, Albany College of Pharmacy & Health Sciences, Albany, NY, USA Trauma Research, St. Joseph's Hospital and Medical Center, Phoenix, AZ, USA.
Monique T FonsecaDepartment of Immunology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, SP, Brazil.
Elizabeth A FlatowDepartment of Immunology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, SP, Brazil.
Kevin LewisDepartment of Pharmaceutical Sciences, Albany College of Pharmacy & Health Sciences, Albany, NY, USA.
Alexandre A SteinerDepartment of Pharmaceutical Sciences, Albany College of Pharmacy & Health Sciences, Albany, NY, USA Trauma Research, St. Joseph's Hospital and Medical Center, Phoenix, AZ, USA Department of Immunology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, SP, Brazil asteiner@usp.br.
St. Joseph's Hospital and Medical Center · USUniversidade de São Paulo · BRAlbany College of Pharmacy and Health Sciences · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We tested the hypothesis that development of hypothermia instead of fever in endotoxic shock is consequential to hypoxia. Endotoxic shock was induced by bacterial lipopolysaccharide (LPS, 500 μg kg(-1) i.v.) in rats at an ambient temperature of 22 °C. A β3-adrenergic agonist known to activate metabolic heat production, CL316,243, was employed to evaluate whether thermogenic capacity could be impaired by the fall in oxygen delivery (ḊO2) during endotoxic shock. This possibility was rejected as CL316,243 (0.15 mg kg(-1) i.v.) evoked similar rises in oxygen consumption (V̇O2) in the presence and absence of endotoxic shock. Next, to investigate whether a less severe form of circulatory hypoxia could be triggering hypothermia, the circulating volume of LPS-injected rats was expanded using 6% hetastarch with the intention of improving tissue perfusion and alleviating hypoxia. This intervention attenuated not only the fall in arterial pressure induced by LPS, but also the associated falls in V̇O2 and body temperature. These effects, however, occurred independently of hypoxia, as they were not accompanied by any detectable changes in NAD(+)/NADH ratios. Further experimentation revealed that even the earliest drops in cardiac output and ḊO2 during endotoxic shock did not precede the reduction in V̇O2 that brings about hypothermia. In fact, ḊO2 and V̇O2 fell in such a synchrony that the ḊO2/V̇O2 ratio remained unaffected. Only when hypothermia was prevented by exposure to a warm environment (30 °C) did an imbalance in the ḊO2/V̇O2 ratio become evident, and such an imbalance was associated with reductions in the renal and hypothalamic NAD(+)/NADH ratios. In conclusion, hypometabolism and hypothermia in endotoxic shock are not consequential to hypoxia but serve as a pre-emptive strategy to avoid hypoxia in this model.

Indexed as

Oxygen ConsumptionThermogenesisAnimalsCardiac OutputEnergy MetabolismHypothermiaMaleNADOxygenRatsRats, WistarShock, SepticNADOxygen

Identifiers

PMID24951620
PMCPMC4192710
OpenAlexW2168531458

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.