Evidence map›Paper›PMID 25589263›Full record

ReviewComprehensive Physiology2015

Human cardiovascular responses to passive heat stress.

Craig G Crandall, Thad E Wilson

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Comprehensive Physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
142citing papers in PubMed, 5 pooled it
–field-weighted citation impact
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

142 citing papers in PubMed, 5 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Trial
  7. Trial
  8. Trial
  9. Glomerular filtration rate reserve is reduced during mild passive heat stress in healthy young adults.American journal of physiology. Regulatory, integrative and comparative physiology · 2022
    Trial
  10. Trial
  11. Trial
  12. Trial
  13. Trial
  14. Trial
  15. Heat therapy promotes the expression of angiogenic regulators in human skeletal muscle.American journal of physiology. Regulatory, integrative and comparative physiology · 2016
    Trial
  16. Trial
  17. Article
  18. Review
  19. Article
  20. Article

82 more citing papers are in PubMed but not listed here.

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

2 authors.

Craig G CrandallInstitute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas and University of Texas Southwestern Medical Center, Dallas, Texas Marian University College of Osteopathic Medicine, Indianapolis, Indiana.
Thad E Wilson

Funding

Exercise in Burn Survivors - Administrative Supplement for EquipmentR01GM068865 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI CRANDALL, CRAIG G · 2003 to 2023
$7.0M
HYPERTHERMIA EFFECTS ON HUMAN BAROFLEX FUNCTIONR01HL061388 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI CRANDALL, CRAIG G · 1999 to 2011
$2.4M
NHLBI NIH HHS R01 HL061388NIGMS NIH HHS R01 GM068865
6 · The paper itself

Abstract

Heat stress increases human morbidity and mortality compared to normothermic conditions. Many occupations, disease states, as well as stages of life are especially vulnerable to the stress imposed on the cardiovascular system during exposure to hot ambient conditions. This review focuses on the cardiovascular responses to heat stress that are necessary for heat dissipation. To accomplish this regulatory feat requires complex autonomic nervous system control of the heart and various vascular beds. For example, during heat stress cardiac output increases up to twofold, by increases in heart rate and an active maintenance of stroke volume via increases in inotropy in the presence of decreases in cardiac preload. Baroreflexes retain the ability to regulate blood pressure in many, but not all, heat stress conditions. Central hypovolemia is another cardiovascular challenge brought about by heat stress, which if added to a subsequent central volumetric stress, such as hemorrhage, can be problematic and potentially dangerous, as syncope and cardiovascular collapse may ensue. These combined stresses can compromise blood flow and oxygenation to important tissues such as the brain. It is notable that this compromised condition can occur at cardiac outputs that are adequate during normothermic conditions but are inadequate in heat because of the increased systemic vascular conductance associated with cutaneous vasodilation. Understanding the mechanisms within this complex regulatory system will allow for the development of treatment recommendations and countermeasures to reduce risks during the ever-increasing frequency of severe heat events that are predicted to occur.

Indexed as

BaroreflexCardiovascular SystemCerebrovascular CirculationHeat Stress DisordersHemodynamicsHumansMuscle, SkeletalRenal CirculationSplanchnic Circulation

Identifiers

PMID25589263
PMCPMC4950975

What OpenQuestion holds

Textmetadata
LicenceTDM
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.