scholarly journals Active and passive heat stress similarly compromise tolerance to a simulated hemorrhagic challenge

2014 ◽  
Vol 307 (7) ◽  
pp. R822-R827 ◽  
Author(s):  
J. Pearson ◽  
R. A. I. Lucas ◽  
Z. J. Schlader ◽  
J. Zhao ◽  
D. Gagnon ◽  
...  
Keyword(s):  
Heat Stress ◽  
Skin Temperature ◽  
Lower Body Negative Pressure ◽  
Stress Index ◽  
Lower Body ◽  
Cumulative Stress ◽  
Hot Environment ◽  
Simulated Hemorrhage ◽  
Exercise Induced ◽  
Skin Temperatures

Passive heat stress increases core and skin temperatures and reduces tolerance to simulated hemorrhage (lower body negative pressure; LBNP). We tested whether exercise-induced heat stress reduces LBNP tolerance to a greater extent relative to passive heat stress, when skin and core temperatures are similar. Eight participants (6 males, 32 ± 7 yr, 176 ± 8 cm, 77.0 ± 9.8 kg) underwent LBNP to presyncope on three separate and randomized occasions: 1) passive heat stress, 2) exercise in a hot environment (40°C) where skin temperature was moderate (36°C, active 36), and 3) exercise in a hot environment (40°C) where skin temperature was matched relative to that achieved during passive heat stress (∼38°C, active 38). LBNP tolerance was quantified using the cumulative stress index (CSI). Before LBNP, increases in core temperature from baseline were not different between trials (1.18 ± 0.20°C; P > 0.05). Also before LBNP, mean skin temperature was similar between passive heat stress (38.2 ± 0.5°C) and active 38 (38.2 ± 0.8°C; P = 0.90) trials, whereas it was reduced in the active 36 trial (36.6 ± 0.5°C; P ≤ 0.05 compared with passive heat stress and active 38). LBNP tolerance was not different between passive heat stress and active 38 trials (383 ± 223 and 322 ± 178 CSI, respectively; P = 0.12), but both were similarly reduced relative to active 36 (516 ± 147 CSI, both P ≤ 0.05). LBNP tolerance is not different between heat stresses induced either passively or by exercise in a hot environment when skin temperatures are similarly elevated. However, LBNP tolerance is influenced by the magnitude of the elevation in skin temperature following exercise induced heat stress.

scholarly journals Small reductions in skin temperature after onset of a simulated hemorrhagic challenge improve tolerance in exercise heat-stressed individuals

2018 ◽  
Vol 315 (3) ◽  
pp. R539-R546
Author(s):  
Claire E. Trotter ◽  
Faith K. Pizzey ◽  
Philip M. Batterson ◽  
Robert A. Jacobs ◽  
James Pearson
Keyword(s):  
Heat Stress ◽  
Mean Arterial Pressure ◽  
Skin Temperature ◽  
Healthy Subjects ◽  
Lower Body Negative Pressure ◽  
Stress Index ◽  
Lower Body ◽  
Vascular Conductance ◽  
Cumulative Stress ◽  
Cutaneous Vascular Conductance

We investigated whether small reductions in skin temperature 60 s after the onset of a simulated hemorrhagic challenge would improve tolerance to lower body negative pressure (LBNP) after exercise heat stress. Eleven healthy subjects completed two trials (High and Reduced). Subjects cycled at ~55% maximal oxygen uptake wearing a warm water-perfused suit until core temperatures increased by ~1.2°C before lying supine and undergoing LBNP to presyncope. LBNP tolerance was quantified as cumulative stress index (CSI; product of each LBNP level multiplied by time; mmHg·min). Skin temperature was similarly elevated from baseline before LBNP and remained elevated 60 s after the onset of LBNP in both High (37.72 ± 0.52°C) and Reduced (37.95 ± 0.54°C) trials (both P < 0.0001). At 60%CSI skin temperature remained elevated in the High trial (37.51 ± 0.56°C) but was reduced to 34.97 ± 0.72°C by the water-perfused suit in the Reduced trial ( P < 0.0001 between trials). Cutaneous vascular conductance was not different between trials [High: 1.57 ± 0.43 vs. Reduced: 1.39 ± 0.38 arbitrary units (AU)/mmHg; P = 0.367] before LBNP but decreased to 0.67 ± 0.19 AU/mmHg at 60%CSI in the Reduced trial while remaining unchanged in the High trial ( P = 0.002 between trials). CSI was higher in the Reduced (695 ± 386 mmHg·min) relative to the High (441 ± 290 mmHg·min; P = 0.023) trial. Mean arterial pressure was not different between trials at presyncope (High: 62 ± 10 vs. Reduced: 62 ± 9 mmHg; P = 0.958). Small reductions in skin temperature after the onset of a simulated hemorrhagic challenge improve LBNP tolerance after exercise heat stress. This may have important implications regarding treatment of an exercise heat-stressed individual (e.g., soldier) who has experienced a hemorrhagic injury.

The magnitude of heat stress-induced reductions in cerebral perfusion does not predict heat stress-induced reductions in tolerance to a simulated hemorrhage

2013 ◽  
Vol 114 (1) ◽  
pp. 37-44 ◽  
Author(s):  
Joshua F. Lee ◽  
Michelle L. Harrison ◽  
Skyler R. Brown ◽  
R. Matthew Brothers
Keyword(s):  
Heat Stress ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Cerebral Perfusion ◽  
Lower Body Negative Pressure ◽  
Small Difference ◽  
Blood Velocity ◽  
Stress Index ◽  
Cumulative Stress ◽  
Simulated Hemorrhage

The mechanisms responsible for heat stress-induced reductions in tolerance to a simulated hemorrhage are unclear. Although a high degree of variability exists in the level of reduction in tolerance amongst individuals, syncope will always occur when cerebral perfusion is inadequate. This study tested the hypothesis that the magnitude of reduction in cerebral perfusion during heat stress is related to the reduction in tolerance to a lower body negative pressure (LBNP) challenge. On different days (one during normothermia and the other after a 1.5°C rise in internal temperature), 20 individuals were exposed to a LBNP challenge to presyncope. Tolerance was quantified as a cumulative stress index, and the difference in cumulative stress index between thermal conditions was used to categorize individuals most (large difference) and least (small difference) affected by the heat stress. Cerebral perfusion, as indexed by middle cerebral artery blood velocity, was reduced during heat stress compared with normothermia ( P < 0.001); however, the magnitude of reduction did not differ between groups ( P = 0.51). In the initial stage of LBNP during heat stress (LBNP 20 mmHg), middle cerebral artery blood velocity and end-tidal Pco2 were lower; whereas, heart rate was higher in the large difference group compared with small difference group ( P < 0.05 for all). These data indicate that variability in heat stress-induced reductions in tolerance to a simulated hemorrhage is not related to reductions in cerebral perfusion in this thermal condition. However, responses affecting cerebral perfusion during LBNP may explain the interindividual variability in tolerance to a simulated hemorrhage when heat stressed.

Skin surface cooling improves orthostatic tolerance in normothermic individuals

2004 ◽  
Vol 286 (1) ◽  
pp. R199-R205 ◽  
Author(s):  
S. Durand ◽  
J. Cui ◽  
K. D. Williams ◽  
C. G. Crandall
Keyword(s):  
Cerebral Blood Flow Velocity ◽  
Lower Body Negative Pressure ◽  
Skin Surface ◽  
Tolerance Test ◽  
Stress Index ◽  
Plasma Norepinephrine ◽  
Orthostatic Tolerance ◽  
Lower Body ◽  
Surface Cooling ◽  
Cumulative Stress

Previous studies suggest that skin surface cooling (SSC) preserves orthostatic tolerance; however, this hypothesis has not been experimentally tested. Thus the purpose of this project was to identify whether SSC improves orthostatic tolerance in otherwise normothermic individuals. Eight subjects underwent two presyncope limited graded lower-body negative pressure (LBNP) tolerance tests. On different days, and randomly assigned, LBNP tolerance was assessed under control conditions and during SSC (perfused 16°C water through tube-lined suit worn by each subject). Orthostatic tolerance was significantly elevated in each individual due to SSC, as evidenced by a significant increase in a standardized cumulative stress index (normothermia 564 ± 58 mmHg·min; SSC 752 ± 58 mmHg·min; P < 0.05). At most levels of LBNP, blood pressure during the SSC tolerance test was significantly greater than during the control test. Furthermore, the reduction in cerebral blood flow velocity was attenuated during some of the early stages of LBNP for the SSC trial. Plasma norepinephrine concentrations were significantly higher during LBNP with SSC, suggesting that SSC may improve orthostatic tolerance through increased sympathetic activity. These data demonstrate that SSC is effective in improving orthostatic tolerance in otherwise normothermic individuals.

scholarly journals Impact of environmental stressors on tolerance to hemorrhage in humans

2019 ◽  
Vol 316 (2) ◽  
pp. R88-R100 ◽  
Author(s):  
Craig G. Crandall ◽  
Caroline A. Rickards ◽  
Blair D. Johnson
Keyword(s):  
Heat Stress ◽  
Blood Loss ◽  
Cause Of Death ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Environmental Stressors ◽  
Lower Body ◽  
Physiological Conditions ◽  
Exercise Induced ◽  
The Impact

Hemorrhage is a leading cause of death in military and civilian settings, and ~85% of potentially survivable battlefield deaths are hemorrhage-related. Soldiers and civilians are exposed to a number of environmental and physiological conditions that have the potential to alter tolerance to a hemorrhagic insult. The objective of this review is to summarize the known impact of commonly encountered environmental and physiological conditions on tolerance to hemorrhagic insult, primarily in humans. The majority of the studies used lower body negative pressure (LBNP) to simulate a hemorrhagic insult, although some studies employed incremental blood withdrawal. This review addresses, first, the use of LBNP as a model of hemorrhage-induced central hypovolemia and, then, the effects of the following conditions on tolerance to LBNP: passive and exercise-induced heat stress with and without hypohydration/dehydration, exposure to hypothermia, and exposure to altitude/hypoxia. An understanding of the effects of these environmental and physiological conditions on responses to a hemorrhagic challenge, including tolerance, can enable development and implementation of targeted strategies and interventions to reduce the impact of such conditions on tolerance to a hemorrhagic insult and, ultimately, improve survival from blood loss injuries.

scholarly journals Hypercapnia-induced increases in cerebral blood flow do not improve lower body negative pressure tolerance during hyperthermia

2013 ◽  
Vol 305 (6) ◽  
pp. R604-R609 ◽  
Author(s):  
Rebekah A. I. Lucas ◽  
James Pearson ◽  
Zachary J. Schlader ◽  
Craig G. Crandall
Keyword(s):  
Negative Pressure ◽  
Cerebral Perfusion ◽  
Lower Body Negative Pressure ◽  
Blood Velocity ◽  
Stress Index ◽  
Gas Mixture ◽  
Lower Body ◽  
Cumulative Stress ◽  
Pressure Tolerance ◽  
End Tidal

Heat-related decreases in cerebral perfusion are partly the result of ventilatory-related reductions in arterial CO2 tension. Cerebral perfusion likely contributes to an individual's tolerance to a challenge like lower body negative pressure (LBNP). Thus increasing cerebral perfusion may prolong LBNP tolerance. This study tested the hypothesis that a hypercapnia-induced increase in cerebral perfusion improves LBNP tolerance in hyperthermic individuals. Eleven individuals (31 ± 7 yr; 75 ± 12 kg) underwent passive heat stress (increased intestinal temperature ∼1.3°C) followed by a progressive LBNP challenge to tolerance on two separate days (randomized). From 30 mmHg LBNP, subjects inhaled either (blinded) a hypercapnic gas mixture (5% CO2, 21% oxygen, balanced nitrogen) or room air (SHAM). LBNP tolerance was quantified via the cumulative stress index (CSI). Mean middle cerebral artery blood velocity (MCAvmean,) and end-tidal CO2 (PetCO2) were also measured. CO2 inhalation of 5% increased PetCO2 at ∼40 mmHg LBNP (by 16 ± 4 mmHg) and at LBNP tolerance (by 18 ± 5 mmHg) compared with SHAM ( P < 0.01). Subsequently, MCAvmean was higher in the 5% CO2 trial during ∼40 mmHg LBNP (by 21 ± 12 cm/s, ∼31%) and at LBNP tolerance (by 18 ± 10 cm/s, ∼25%) relative to the SHAM ( P < 0.01). However, hypercapnia-induced increases in MCAvmean did not alter LBNP tolerance (5% CO2 CSI: 339 ± 155 mmHg × min; SHAM CSI: 273 ± 158 mmHg × min; P = 0.26). These data indicate that inhaling a hypercapnic gas mixture increases cerebral perfusion during LBNP but does not improve LBNP tolerance when hyperthermic.

Women have lower tolerance to lower body negative pressure than men

1996 ◽  
Vol 80 (4) ◽  
pp. 1138-1143 ◽  
Author(s):  
D. D. White ◽  
R. W. Gotshall ◽  
A. Tucker
Keyword(s):  
Negative Pressure ◽  
Heart Rate Response ◽  
Lower Body Negative Pressure ◽  
Cardiovascular Response ◽  
Stress Index ◽  
Lower Body ◽  
Men And Women ◽  
Cumulative Stress ◽  
Cardiovascular Variables ◽  
Lower Tolerance

Studies of the cardiovascular response to lower body negative pressure (LBNP) in men and women have suggested that women may have less tolerance to LBNP than men, although tolerance per se was not determined. To investigate the effect of gender on tolerance to LBNP, 10 men 10 women were subjected to increasing levels of LBNP until presyncopal symptoms developed. The cumulative stress index (CSI) score was determined, as were cardiovascular variables. Women had 62% less tolerance to LBNP with a CSI of 412 +/- 43 mmHg/min compared with a CSI of 1,070 +/- 149 mmHg/min for men. Cardiovascular changes associated with LBNP were similar for men and women when expressed relative to the occurrence of presyncope, but women had a higher heart rate response when the data were expressed at absolute levels of LBNP (-30 and -50 mmHg LBNP). Thus men and women had similar cardiovascular adjustments to the LBNP, with the changes in women occurring lower levels of LBNP. These data are important in a consideration of the development of antigravitational countermeasures for women. These data raise questions as to the manner in which blood pools within the lower body in men and women under LBNP.

Comparative Efficacy of Physiological Responses and Skin Temperatures in Indigenous and Crossbred Cattle Supplemented with Chlorophytum borivilianum in Summer Season

2021 ◽  
Author(s):  
Pooja Devi ◽  
Mahendra Singh ◽  
Yallappa M. Somagond ◽  
A.K. Roy
Keyword(s):  
Heat Stress ◽  
Skin Temperature ◽  
Physiological Responses ◽  
High Dose ◽  
Crossbred Cattle ◽  
Comparative Efficacy ◽  
Production Potential ◽  
Chlorophytum Borivilianum ◽  
Humidity Index ◽  
Skin Temperatures

Background: Heat stress causes oxidative stress and declines milk production potential of cows. The physiological responses and skin temperature of heat stressed animals are good indices for deterring the heat stress. The efficacy of medicinal herb Chlorophytum borivilianum (CB) was tested in lowering the rise in values of physiological responses and skin temperature in crossbred vis a vis Indigenous cows. Methods: Eighteen Tharparkar (TP) and Crossbred KF cows in mid-lactation were given; No supplement (control), a low (T1, n=6) and a high dose (T2, n=6) of CB @ 40 and 80 mg/kg BW/day, respectively for 90 days during hot-humid season. Respiration rate (RR), pulse rate (PR), rectal temperature (RT) and skin temperature (ST) was recorded at the site of forehead, neck, rear body, and udder surface in the morning and afternoon at weekly intervals. Temperature-humidity index (THI) was calculated to assess the degree of thermal stress in animals. Result: Physiological responses and skin temperatures were higher (p less than 0.01) in the afternoon than morning intervals in TP and KF cows. CB feeding significantly lowered physiological responses and ST (p less than 0.01) in high dose as compared to low dose. It was concluded that CB feeding @ 80 mg/kg BW/day effectively alleviates the heat stress. Indigenous cows were found more heat tolerant in comparison to crossbred cows.

scholarly journals Hemorrhage simulated by lower body negative pressure provokes an oxidative stress response in healthy young adults

2019 ◽  
Vol 244 (3) ◽  
pp. 272-278
Author(s):  
Flora S Park ◽  
Victoria L Kay ◽  
Justin D Sprick ◽  
Alexander J Rosenberg ◽  
Garen K Anderson ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Human Subjects ◽  
Oxidative Stress Response ◽  
Lower Body ◽  
Healthy Human ◽  
Healthy Human Subjects ◽  
Simulated Hemorrhage

Hemorrhage is a leading cause of potentially preventable death in both civilian and military trauma settings. Lower body negative pressure (LBNP) is a validated, non-invasive, and reproducible approach to simulate hemorrhage by inducing central hypovolemia in healthy conscious humans. The oxidative stress response to simulated hemorrhage via LBNP has not been quantified. We hypothesized that systemic markers of oxidative stress would increase with application of maximal, pre-syncopal limited LBNP. Fifteen healthy human subjects (11 M/4 F; age 27 ± 1 y) were recruited for a single LBNP experiment to presyncope (chamber pressure was progressively reduced every 5-min in a stepwise manner). Heart rate was assessed via ECG, arterial pressure and stroke volume (SV) were measured continuously via finger photoplethysmography, muscle oxygen saturation (SmO2) was measured via near-infrared spectroscopy, and venous blood samples were collected at baseline and presyncope. Plasma samples were analyzed for F2-isoprostanes (F2-IsoP), a global marker of oxidative stress. The magnitude of central hypovolemia, indexed by the maximal decrease (%Δ) in SV, ranged from 27 to 74% (53.5 ± 3.9%; P < 0.001), and mean arterial pressure (MAP) decreased by 12.6 ± 2.6% ( P < 0.001 vs. pre-LBNP baseline). F2-IsoP increased by 28.5 ± 11.6% ( P = 0.05) from baseline (24 ± 2 pg/mL) to presyncope (29 ± 3 pg/mL). The increase in F2-IsoP was not associated with %Δ SV ( r = 0.21, P = 0.46), %Δ MAP ( r = 0.05, P = 0.86), %Δ SmO2 ( r = 0.05, P = 0.90), or the maximum level of LBNP attained ( r = 0.35, P = 0.20). Simulated hemorrhage induced by LBNP to presyncope elicited an increase in oxidative stress, but this response was not associated with the magnitude of central hypovolemia, hypotension, or the decrease in peripheral muscle tissue oxygen saturation. These findings have important implications for the study of hemorrhage using LBNP, and future investigations of interventions targeting oxidative stress. Impact statement We characterize the systemic oxidative stress response in young, healthy human subjects with exposure to simulated hemorrhage via application of lower body negative pressure (LBNP). Prior work has demonstrated that LBNP and actual blood loss evoke similar hemodynamic and immune responses (i.e. white blood cell count), but it is unknown whether LBNP elicits oxidative stress resembling that produced by blood loss. We show that LBNP induces a 29% increase in F2-isoprostanes, a systemic marker of oxidative stress. The findings of this investigation may have important implications for the study of hemorrhage using LBNP, including future assessments of targeted interventions that may reduce oxidative stress, such as novel fluid resuscitation approaches.

scholarly journals Heat-stress-induced changes in central venous pressure do not explain interindividual differences in orthostatic tolerance during heat stress

2011 ◽  
Vol 110 (5) ◽  
pp. 1283-1289 ◽  
Author(s):  
R. Matthew Brothers ◽  
David M. Keller ◽  
Jonathan E. Wingo ◽  
Matthew S. Ganio ◽  
Craig G. Crandall
Keyword(s):  
Blood Pressure ◽  
Heat Stress ◽  
Central Venous Pressure ◽  
Blood Pressure Control ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Pressure Control ◽  
Stress Index ◽  
Central Venous ◽  
The Difference

The extent to which heat stress compromises blood pressure control is variable among individuals, with some individuals becoming very intolerant to a hypotensive challenge, such as lower body negative pressure (LBNP) while heat stressed, while others are relatively tolerant. Heat stress itself reduces indexes of ventricular filling pressure, including central venous pressure, which may be reflective of reductions in tolerance in this thermal condition. This study tested the hypothesis that the magnitude of the reduction in central venous pressure in response to heat stress alone is related to the subsequent decrement in LBNP tolerance. In 19 subjects, central hypovolemia was imposed via LBNP to presyncope in both normothermic and heat-stress conditions. Tolerance to LBNP was quantified using a cumulative stress index (CSI), and the difference between normothermic CSI and heat-stress CSI was calculated for each individual. The eight individuals with the greatest CSI difference between normothermic and heat-stress tolerances (LargeDif), and the eight individuals with the smallest CSI difference (SmallDif), were grouped together. By design, the difference in CSI between thermal conditions was greater in the LargeDif group (969 vs. 382 mmHg × min; P < 0.001). Despite this profound difference in the effect of heat stress in decreasing LBNP tolerance between groups, coupled with no difference in the rise in core body temperatures to the heat stress (LargeDif, 1.4 ± 0.1°C vs. SmallDif, 1.4 ± 0.1°C; interaction P = 0.89), the reduction in central venous pressure during heat stress alone was similar between groups (LargeDif: 5.7 ± 1.9 mmHg vs. SmallDif: 5.2 ± 2.0 mmHg; interaction P = 0.85). Contrary to the proposed hypothesis, differences in blood pressure control during LBNP are not related to differences in the magnitude of the heat-stress-induced reductions in central venous pressure.

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