Evidence map›Paper›PMID 30231210›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2019

Hemostatic responses to exercise, dehydration, and simulated bleeding in heat-stressed humans.

Matthew A Borgman, Morten Zaar, James K Aden, Zachary J Schlader, Daniel Gagnon, Eric Rivas, Jena Kern, Natalie J Koons, Victor A Convertino, Andrew P Cap and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

12 citing papers in PubMed, 29 citations in OpenAlex.

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  11. American journal of physiology. Regulatory, integrative and comparative physiology · 2020
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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

11 authors at 6 institutions in 2 countries.

Matthew A BorgmanUnited States Army Institute of Surgical Research, Fort Sam Houston, Texas.
Morten ZaarUnited States Army Institute of Surgical Research, Fort Sam Houston, Texas.
James K AdenDepartment of Pediatrics, Brooke Army Medical Center, Fort Sam Houston, Texas.
Zachary J SchladerDepartment of Exercise and Nutritional Sciences, Center for Research and Education in Special Environments, University of Buffalo , New York.
Daniel GagnonMontreal Heart Institute and University of Montreal , Canada.ORCID 0000-0001-5396-9489
Eric RivasDepartment of Kinesiology & Sport Management, Texas Tech University , Lubbock, Texas.ORCID 0000-0002-4657-8292
Jena KernInstitute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital of Dallas , Dallas, Texas.
Natalie J KoonsUnited States Army Institute of Surgical Research, Fort Sam Houston, Texas.
Victor A ConvertinoUnited States Army Institute of Surgical Research, Fort Sam Houston, Texas.
Andrew P CapUnited States Army Institute of Surgical Research, Fort Sam Houston, Texas.
Craig CrandallInstitute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital of Dallas , Dallas, Texas.ORCID 0000-0001-7792-9713
United States Army Institute of Surgical Research · USBrooke Army Medical Center · USTexas Health Dallas · USMontreal Heart Institute · CATexas Tech University · USUniversity at Buffalo, State University of New York · 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 R01 HL061388
6 · The paper itself

Abstract

Heat stress followed by an accompanying hemorrhagic challenge may influence hemostasis. We tested the hypothesis that hemostatic responses would be increased by passive heat stress, as well as exercise-induced heat stress, each with accompanying central hypovolemia to simulate a hemorrhagic insult. In aim 1, subjects were exposed to passive heating or normothermic time control, each followed by progressive lower-body negative pressure (LBNP) to presyncope. In aim 2 subjects exercised in hyperthermic environmental conditions, with and without accompanying dehydration, each also followed by progressive LBNP to presyncope. At baseline, pre-LBNP, and post-LBNP (<1, 30, and 60 min), hemostatic activity of venous blood was evaluated by plasma markers of hemostasis and thrombelastography. For aim 1, both hyperthermic and normothermic LBNP (H-LBNP and N-LBNP, respectively) resulted in higher levels of factor V, factor VIII, and von Willebrand factor antigen compared with the time control trial (all P < 0.05), but these responses were temperature independent. Hyperthermia increased fibrinolysis [clot lysis 30 min after the maximal amplitude reflecting clot strength (LY

Indexed as

AdultArterial PressureDehydrationExerciseHeat-Shock ResponseHeat Stress DisordersHemorrhageHemostasisHot TemperatureHumansHyperthermia, InducedHypovolemiaLower Body Negative PressureMalecoagulationfibrinolysishyperthermiahypovolemialower body negative pressure

Identifiers

PMID30231210
PMCPMC6397353
OpenAlexW2889871423

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.