scholarly journals Heat stress does not augment ventilatory responses to presyncopal limited lower body negative pressure

2013 ◽  
Vol 98 (7) ◽  
pp. 1156-1163 ◽  
Author(s):  
J. Pearson ◽  
M. S. Ganio ◽  
R. A. I. Lucas ◽  
T. G. Babb ◽  
C. G. Crandall
Keyword(s):  
Heat Stress ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Ventilatory Responses

scholarly journals Sweat loss during heat stress contributes to subsequent reductions in lower-body negative pressure tolerance

2012 ◽  
Vol 98 (2) ◽  
pp. 473-480 ◽  
Author(s):  
Rebekah A. I. Lucas ◽  
Matthew S. Ganio ◽  
James Pearson ◽  
Craig G. Crandall
Keyword(s):  
Heat Stress ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Sweat Loss ◽  
Pressure Tolerance

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.

Divergent roles of plasma osmolality and the baroreflex on sweating and skin blood flow

2012 ◽  
Vol 302 (5) ◽  
pp. R634-R642 ◽  
Author(s):  
Aaron G. Lynn ◽  
Daniel Gagnon ◽  
Konrad Binder ◽  
Robert C. Boushel ◽  
Glen P. Kenny
Keyword(s):  
Blood Flow ◽  
Heat Stress ◽  
Core Temperature ◽  
Skin Blood Flow ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Plasma Osmolality ◽  
Whole Body ◽  
Lower Body ◽  
Change In Mean

Plasma hyperosmolality and baroreceptor unloading have been shown to independently influence the heat loss responses of sweating and cutaneous vasodilation. However, their combined effects remain unresolved. On four separate occasions, eight males were passively heated with a liquid-conditioned suit to 1.0°C above baseline core temperature during a resting isosmotic state (infusion of 0.9% NaCl saline) with (LBNP) and without (CON) application of lower-body negative pressure (−40 cmH2O) and during a hyperosmotic state (infusion of 3.0% NaCl saline) with (LBNP + HYP) and without (HYP) application of lower-body negative pressure. Forearm sweat rate (ventilated capsule) and skin blood flow (laser-Doppler), as well as core (esophageal) and mean skin temperatures, were measured continuously. Plasma osmolality increased by ∼10 mosmol/kgH2O during HYP and HYP + LBNP conditions, whereas it remained unchanged during CON and LBNP ( P ≤ 0.05). The change in mean body temperature (0.8 × core temperature + 0.2 × mean skin temperature) at the onset threshold for increases in cutaneous vascular conductance (CVC) was significantly greater during LBNP (0.56 ± 0.24°C) and HYP (0.69 ± 0.36°C) conditions compared with CON (0.28 ± 0.23°C, P ≤ 0.05). Additionally, the onset threshold for CVC during LBNP + HYP (0.88 ± 0.33°C) was significantly greater than CON and LBNP conditions ( P ≤ 0.05). In contrast, onset thresholds for sweating were not different during LBNP (0.50 ± 0.18°C) compared with CON (0.46 ± 0.26°C, P = 0.950) but were elevated ( P ≤ 0.05) similarly during HYP (0.91 ± 0.37°C) and LBNP + HYP (0.94 ± 0.40°C). Our findings show an additive effect of hyperosmolality and baroreceptor unloading on the onset threshold for increases in CVC during whole body heat stress. In contrast, the onset threshold for sweating during heat stress was only elevated by hyperosmolality with no effect of the baroreflex.

scholarly journals Cerebral vasoreactivity: impact of heat stress and lower body negative pressure

2014 ◽  
Vol 24 (3) ◽  
pp. 135-141 ◽  
Author(s):  
Joshua F. Lee ◽  
Kevin M. Christmas ◽  
Michelle L. Harrison ◽  
Kiyoung Kim ◽  
Chansol Hurr ◽  
...  
Keyword(s):  
Heat Stress ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Cerebral Vasoreactivity

Neurohormonal responses to oscillatory lower body negative pressure in healthy subjects

2021 ◽  
Author(s):  
Akanksha Singh ◽  
Shival Srivastav ◽  
Kavita Yadav ◽  
Dinu S. Chandran ◽  
Ashok Kumar Jaryal ◽  
...  
Keyword(s):  
Negative Pressure ◽  
Healthy Subjects ◽  
Lower Body Negative Pressure ◽  
Lower Body

Bradykinin has no acute effect on the response of forearm blood flow to sympathetic stimulation in man

1990 ◽  
Vol 78 (4) ◽  
pp. 399-401 ◽  
Author(s):  
M. J. Cullen ◽  
J. R. Cockcroft ◽  
D. J. Webb
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Negative Pressure ◽  
Enzyme Inhibitor ◽  
Lower Body Negative Pressure ◽  
Acute Effect ◽  
Acute Administration ◽  
Lower Body ◽  
Resistance Vessels ◽  
Sympathetic Responses

1. Six healthy male subjects received 0.9% (w/v) NaCl (saline) followed by incremental doses of bradykinin (1, 3 and 10 pmol/min), via the left brachial artery. Blood flow and the response of blood flow to lower-body negative pressure were measured in both forearms during infusion of saline and each dose of bradykinin. 2. Bradykinin produced a moderate and dose-dependent increase in blood flow in the infused, but not the non-infused, forearm. Lower-body negative pressure produced an approximately 15–20% reduction in blood flow in both forearms, and this response was unaffected by local infusion of bradykinin. 3. Bradykinin, in contrast to angiotensin II, had no acute effect on peripheral sympathetic responses to lower-body negative pressure. We conclude that, in forearm resistance vessels in man, withdrawal of angiotensin II, rather than accumulation of bradykinin, is likely to account for the attenuation of peripheral sympathetic responses after acute administration of a converting-enzyme inhibitor.

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