Study2019

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

Borgman MA, Zaar M, Aden JK, Schlader ZJ, Gagnon D, Rivas E, Kern J, Koons NJ, Convertino VA, Cap AP, Crandall C

American journal of physiology. Regulatory, integrative and comparative physiology · 22 citations

How it was studied

Design
Controlled clinical trial (classified by our AI screen)
Studied in
People
Main outcome
Health markers and function

Who paid for it

Funding
Independent funding
Government
U.S. Department of Defense
Government
National Institutes of Health
Government
National Heart, Lung, and Blood Institute
Government
U.S. Department of Defense (DOD)
Government
NHLBI NIH HHS
Grants
U.S. Department of Defense (W81XWH1210152); National Heart, Lung, and Blood Institute (R01HL061388); National Institutes of Health (HL‐61388)

Based on 5 listed funder(s).

Publication

Published
2018-09-19 · Am J Physiol Regul Integr Comp Physiol · vol. 316 · issue 2 · pp. R145–R156
Publisher
American Physiological Society
Cited
32 citations · more than 79% of similar papers · 1.3× the field average
References
45 works
Access
Open access (repository copy)
Research areas
Thermoregulation and physiological responses · Climate Change and Health Impacts · Trauma, Hemostasis, Coagulopathy, Resuscitation
Keywords
Presyncope, Fibrinolysis, Medicine, Hyperthermia, Hemostasis, Hypovolemia, Internal medicine, Thromboelastography, Anesthesia, Blood pressure, Platelet, Heart rate
MeSH
humans, dehydration, heat stress disorders, hemorrhage, hypovolemia, lower body negative pressure, exercise, hyperthermia, induced, heat-shock response, hemostasis, adult, male, hot temperature, arterial pressure

11 authors

From US, CA

  • Matthew A. Borgman · correspondingBrooke Army Medical Center; United States Army Institute of Surgical Research; Joint Base San Antonio
  • Morten ZaarUnited States Army Institute of Surgical Research
  • James Keith AdenBrooke Army Medical Center; Joint Base San Antonio
  • Zachary J. SchladerUniversity at Buffalo, State University of New York
  • Daniel GagnonMontreal Heart Institute; Université de Montréal
  • Eric RivasTexas Tech University

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 (30)] to 5.1% post-LBNP compared with 1.5% (time control) and 2.7% in N-LBNP ( P = 0.05 for main effect). Hyperthermia also potentiated increased platelet counts post-LBNP as follows: 274 K/µl for H-LBNP, 246 K/µl for N-LBNP, and 196 K/µl for time control ( P 30) was increased to 6-10% when subjects were dehydrated compared with an increase to 2-4% when hydrated ( P = 0.05 for treatment). Central hypovolemia via LBNP is a primary driver of hemostasis compared with hyperthermia and dehydration effects. However, hyperthermia does induce significant thrombocytosis and by itself causes an increase in clot lysis. Dehydration associated with exercise-induced heat stress increases clot lysis but does not affect exercise-activated or subsequent hypovolemia-activated hemostasis in hyperthermic humans. Clinical implications of these findings are that quickly restoring a hemorrhaging hypovolemic trauma patient with cold noncoagulant fluids (crystalloids) can have serious deleterious effects on the body's innate ability to form essential clots, and several factors can increase clot lysis, which should therefore be closely monitored.

Abstract via Europe PMC. Copyright remains with the authors or publisher.

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