Evidence map›Paper›PMID 22367508›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2012

Effect of heat stress on cardiac output and systemic vascular conductance during simulated hemorrhage to presyncope in young men.

Matthew S Ganio, Morten Overgaard, Thomas Seifert, Niels H Secher, Pär I Johansson, Martin A S Meyer, Craig G Crandall

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Normothermic central hypovolemia tolerance reflects hyperthermic tolerance.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2014
    Trial
  4. Trial
  5. Trial
  6. Article
  7. Cerebrovascular regulation during heat stress.Experimental physiology · 2026
    Review
  8. Review
  9. Review
  10. Impact of environmental stressors on tolerance to hemorrhage in humans.American journal of physiology. Regulatory, integrative and comparative physiology · 2019
    Article
  11. Article
  12. Mechanisms of orthostatic intolerance during heat stress.Autonomic neuroscience : basic & clinical · 2016
    Review
  13. Instrument to detect syncope and the onset of shock.Proceedings of SPIE--the International Society for Optical Engineering · 2016
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Cerebral oxygenation and hyperthermia.Frontiers in physiology · 2014
    Review
  19. Article
  20. 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

7 authors at 3 institutions in 2 countries.

Matthew S GanioInstitute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital, Dallas, Teaxs 75231, USA.
Morten Overgaard
Thomas Seifert
Niels H Secher
Pär I Johansson
Martin A S Meyer
Craig G Crandall
Rigshospitalet · DKInstitute for Exercise and Environmental Medicine · USSection of Transfusion Medicine Capital Region Blood Bank & Department of Clinical Immunology · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During moderate actual or simulated hemorrhage, as cardiac output decreases, reductions in systemic vascular conductance (SVC) maintain mean arterial pressure (MAP). Heat stress, however, compromises the control of MAP during simulated hemorrhage, and it remains unknown whether this response is due to a persistently high SVC and/or a low cardiac output. This study tested the hypothesis that an inadequate decrease in SVC is the primary contributing mechanism by which heat stress compromises blood pressure control during simulated hemorrhage. Simulated hemorrhage was imposed via lower body negative pressure (LBNP) to presyncope in 11 passively heat-stressed subjects (increase core temperature: 1.2 ± 0.2°C; means ± SD). Cardiac output was measured via thermodilution, and SVC was calculated while subjects were normothermic, heat stressed, and throughout subsequent LBNP. MAP was not changed by heat stress but was reduced to 45 ± 12 mmHg at the termination of LBNP. Heat stress increased cardiac output from 7.1 ± 1.1 to 11.7 ± 2.2 l/min (P < 0.001) and increased SVC from 0.094 ± 0.018 to 0.163 ± 0.032 l·min(-1)·mmHg(-1) (P < 0.001). Although cardiac output at the onset of syncopal symptoms was 37 ± 16% lower relative to pre-LBNP, presyncope cardiac output (7.3 ± 2.0 l/min) was not different than normothermic values (P = 0.46). SVC did not change throughout LBNP (P > 0.05) and at presyncope was 0.168 ± 0.044 l·min(-1)·mmHg(-1). These data indicate that in humans a cardiac output adequate to maintain MAP while normothermic is no longer adequate during a heat-stressed-simulated hemorrhage. The absence of a decrease in SVC at a time of profound reductions in MAP suggests that inadequate control of vascular conductance is a primary mechanism compromising blood pressure control during these conditions.

Indexed as

AdultBlood PressureBody TemperatureCardiac OutputCatecholaminesEpinephrineHeart RateHeat Stress DisordersHemorrhageHumansLower Body Negative PressureMalePulmonary ArterySkin TemperatureSupine PositionSyncopeCatecholaminesEpinephrine

Identifiers

PMID22367508
PMCPMC3330796
OpenAlexW2121804475

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.