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 citas
Cómo se estudió
- Diseño
- Ensayo clínico controlado (clasificado por nuestro filtro de IA)
- Estudiado en
- Personas
- Resultado principal
- Marcadores de salud y funcionamiento
Quién lo pagó
- Financiación
- Financiación independiente
- Gobierno
- U.S. Department of Defense
- Gobierno
- National Institutes of Health
- Gobierno
- National Heart, Lung, and Blood Institute
- Gobierno
- U.S. Department of Defense (DOD)
- Gobierno
- NHLBI NIH HHS
- Subvenciones
- U.S. Department of Defense (W81XWH1210152); National Heart, Lung, and Blood Institute (R01HL061388); National Institutes of Health (HL‐61388)
Según 5 financiadores declarados.
Publicación
- Publicado
- 2018-09-19 · Am J Physiol Regul Integr Comp Physiol · vol. 316 · número 2 · págs. R145–R156
- Editorial
- American Physiological Society
- Citado
- 32 citas · más que el 79% de estudios similares · 1.3× el promedio de su campo
- Referencias
- 45 trabajos
- Acceso
- Acceso abierto (copia en repositorio)
- Áreas de investigación
- Thermoregulation and physiological responses · Climate Change and Health Impacts · Trauma, Hemostasis, Coagulopathy, Resuscitation
- Palabras clave
- 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 autores
- Matthew A. Borgman🇺🇸 · autor de correspondenciaBrooke Army Medical Center; United States Army Institute of Surgical Research; Joint Base San Antonio
- Morten Zaar🇺🇸United States Army Institute of Surgical Research
- James Keith Aden🇺🇸Brooke Army Medical Center; Joint Base San Antonio
- Zachary J. Schlader🇺🇸University at Buffalo, State University of New York
- Daniel Gagnon🇨🇦Montreal Heart Institute; Université de Montréal
- Eric Rivas🇺🇸Texas Tech University
- Jena Kern🇺🇸Texas Health Dallas; Institute for Exercise and Environmental Medicine
- Natalie Jane Koons🇺🇸United States Army Institute of Surgical Research
- Víctor A. Convertino🇺🇸United States Army Institute of Surgical Research
- Andrew P. Cap🇺🇸United States Army Institute of Surgical Research
- Craig G. Crandall🇺🇸Texas Health Dallas; Institute for Exercise and Environmental Medicine; The University of Texas Southwestern Medical Center
Resumen
El texto original del estudio, en el idioma en que se publicó.
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.
Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial.
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