Evidence map›Paper›PMID 25031230›Full record

Trial reportAmerican journal of physiology. Regulatory, integrative and comparative physiology2014

Tissue oxygen saturation during hyperthermic progressive central hypovolemia.

Zachary J Schlader, Eric Rivas, Babs R Soller, Victor A Convertino, Craig G Crandall

Open access · greenAbstract readRandomized Controlled Trial
In one paragraph

Trial report in American journal of physiology. Regulatory, integrative and comparative physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 26% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Mechanisms of orthostatic intolerance during heat stress.Autonomic neuroscience : basic & clinical · 2016
    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 4 institutions in 1 country.

Zachary J SchladerInstitute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital of Dallas, Dallas, Texas, and the University of Texas Southwestern Medical Center, Dallas, Texas;
Eric RivasInstitute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital of Dallas, Dallas, Texas, and the University of Texas Southwestern Medical Center, Dallas, Texas; Department of Kinesiology, Texas Woman's University, Denton, Texas;
Babs R SollerReflectance Medical Incorporated, Westborough, Massachusetts; Department of Anesthesiology, University of Massachusetts Medical School, Worcester, Massachusetts; and.
Victor A ConvertinoU.S. Army Institute of Surgical Research, Fort Sam Houston, Texas.
Craig G CrandallInstitute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital of Dallas, Dallas, Texas, and the University of Texas Southwestern Medical Center, Dallas, Texas; CraigCrandall@texashealth.org.
Southwestern Medical Center · USTexas Woman's University · USUnited States Army Institute of Surgical Research · USUniversity of Massachusetts Chan Medical School · US

Funding

HYPERTHERMIA EFFECTS ON HUMAN BAROFLEX FUNCTIONR01HL061388 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI CRANDALL, CRAIG G · 1999 to 2011
$2.4M
NHLBI NIH HHS HL-61388NIA NIH HHS F32AG-04328
6 · The paper itself

Abstract

During normothermia, a reduction in near-infrared spectroscopy (NIRS)-derived tissue oxygen saturation (So2) is an indicator of central hypovolemia. Hyperthermia increases skin blood flow and reduces tolerance to central hypovolemia, both of which may alter the interpretation of tissue So2 during central hypovolemia. This study tested the hypothesis that maximal reductions in tissue So2 would be similar throughout normothermic and hyperthermic central hypovolemia to presyncope. Ten healthy males (means ± SD; 32 ± 5 yr) underwent central hypovolemia via progressive lower-body negative pressure (LBNP) to presyncope during normothermia (skin temperature ≈34°C) and hyperthermia (+1.2 ± 0.1°C increase in internal temperature via a water-perfused suit, skin temperature ≈39°C). NIRS-derived forearm (flexor digitorum profundus) tissue So2 was measured throughout and analyzed as the absolute change from pre-LBNP. Hyperthermia reduced (P < 0.001) LBNP tolerance by 49 ± 33% (from 16.7 ± 7.9 to 7.2 ± 3.9 min). Pre-LBNP, tissue So2 was similar (P = 0.654) between normothermia (74 ± 5%) and hyperthermia (73 ± 7%). Tissue So2 decreased (P < 0.001) throughout LBNP, but the reduction from pre-LBNP to presyncope was greater during normothermia (-10 ± 6%) than during hyperthermia (-6 ± 5%; P = 0.041). Contrary to our hypothesis, these findings indicate that hyperthermia is associated with a smaller maximal reduction in tissue So2 during central hypovolemia to presyncope.

Indexed as

Oxygen ConsumptionAdultArterial PressureFeverForearmHeart RateHumansHypovolemiaLower Body Negative PressureMaleMuscle, SkeletalOxygenRegional Blood FlowSkinSkin TemperatureSpectroscopy, Near-InfraredOxygenheat stresslower body negative pressuresimulated hemorrhagesyncope

Identifiers

PMID25031230
PMCPMC4166753
OpenAlexW2137377389

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.