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.

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.

scholarly journals Regulation of regional cerebral blood flow during graded reflex-mediated sympathetic activation via lower body negative pressure

2018 ◽  
Vol 125 (6) ◽  
pp. 1779-1786 ◽  
Author(s):  
Jasdeep Kaur ◽  
Jennifer R. Vranish ◽  
Thales C. Barbosa ◽  
Takuro Washio ◽  
Benjamin E. Young ◽  
...  
Keyword(s):  
Blood Flow ◽  
Negative Pressure ◽  
Internal Carotid ◽  
Lower Body Negative Pressure ◽  
Blood Velocity ◽  
Lower Body ◽  
Sympathetic Activation ◽  
Voluntary Hyperventilation ◽  
End Tidal ◽  
Baseline Diameter

The role of the sympathetic nervous system in cerebral blood flow (CBF) regulation remains unclear. Previous studies have primarily measured middle cerebral artery blood velocity to assess CBF. Recently, there has been a transition toward measuring internal carotid artery (ICA) and vertebral artery (VA) blood flow using duplex Doppler ultrasound. Given that the VA supplies autonomic control centers in the brainstem, we hypothesized that graded sympathetic activation via lower body negative pressure (LBNP) would reduce ICA but not VA blood flow. ICA and VA blood flow were measured during two protocols: protocol 1, low-to-moderate LBNP (−10, −20, −30, and −40 Torr) and protocol 2, moderate-to-high LBNP (−30, −50, and −70 Torr). ICA and VA blood flow, diameter, and blood velocity were unaffected up to −40 LBNP. However, −50 and −70 LBNP evoked reductions in ICA and VA blood flow [e.g., −70 LBNP: percent change (%∆)VA-baseline = −27.6 ± 3.0] that were mediated by decreases in both diameter and velocity (e.g., −70 LBNP: %∆VA-baseline diameter = −7.5 ± 1.9 and %∆VA-baseline velocity = −13.6 ± 1.7), which were comparable between vessels. Since hyperventilation during −70 LBNP reduced end-tidal pressure of carbon dioxide ([Formula: see text]), this decrease in [Formula: see text] was matched via voluntary hyperventilation. Reductions in ICA and VA blood flow during hyperventilation alone were significantly smaller than during −70 LBNP and were primarily mediated by decreases in velocity (%∆VA-baseline velocity = −8.6 ± 2.4 and %∆VA-baseline diameter = −0.05 ± 0.56). These data demonstrate that both ICA and VA were unaffected by low-to-moderate sympathetic activation, whereas robust reflex-mediated sympathoexcitation caused similar magnitudes of vasoconstriction in both arteries. Thus, contrary to our hypothesis, the ICA was not preferentially vasoconstricted by sympathetic activation. NEW & NOTEWORTHY Our study demonstrates that moderate-to-high reflex-mediated sympathetic activation with lower body negative pressure (LBNP) decreases internal carotid artery and vertebral artery blood flow via reductions in both vessel diameter and blood velocity. This vasoconstriction was primarily sympathetically mediated as voluntary hyperventilation alone, to isolate the effect of decreases in end-tidal pressure of carbon dioxide that occurred during LBNP, resulted in a significantly smaller vasoconstriction. In contrast to our hypothesis, these data indicate a lack of heterogeneity between the anterior and posterior cerebral circulations in response to sympathoexcitation.

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.

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.

scholarly journals Blunted shear-mediated dilation of the internal but not common carotid artery in response to lower body negative pressure

2018 ◽  
Vol 124 (5) ◽  
pp. 1326-1332 ◽  
Author(s):  
Erika Iwamoto ◽  
Joshua M. Bock ◽  
Darren P. Casey
Keyword(s):  
Negative Pressure ◽  
Cerebral Perfusion ◽  
Carotid Arteries ◽  
Internal Carotid ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Healthy Men ◽  
Sympathetic Nervous ◽  
Internal Carotid Arteries

Shear-mediated dilation in peripheral conduit arteries is blunted with sympathetic nervous system (SNS) activation; however, the effect of SNS activation on shear-mediated dilation in carotid arteries is unknown. We hypothesized that SNS activation reduces shear-mediated dilation in common and internal carotid arteries (CCA and ICA, respectively), and this attenuation is greater in the ICA compared with the CCA. Shear-mediated dilation in the CCA and ICA were measured in nine healthy men (24 ± 1 yr) with and without SNS activation. Shear-mediated dilation was induced by 3 min of hypercapnia (end‐tidal partial pressure of carbon dioxide +10 mmHg from individual baseline); SNS activity was increased with lower body negative pressure (LBNP; −20 mmHg). CCA and ICA measurements were made using Doppler ultrasound during hypercapnia with (LBNP) or without (Control) SNS activation. LBNP trials began with 5 min of LBNP with subjects breathing hypercapnic gas during the final 3 min. Shear-mediated dilation was calculated as the percent rise in peak diameter from baseline diameter. Sympathetic activation attenuated shear-mediated dilation in the ICA (Control vs. LBNP, 5.5 ± 0.7 vs. 1.8 ± 0.4%, P < 0.01), but not in the CCA (5.1 ± 1.2 vs. 4.2 ± 1.0%, P = 0.31). Moreover, absolute reduction in shear-mediated dilation via SNS activation was greater in the ICA than the CCA (−3.6 ± 0.7 vs. −0.9 ± 0.8%, P = 0.02). Our data indicate that shear-mediated dilation is attenuated during LBNP to a greater extent in the ICA compared with the CCA. These results potentially provide insight into the role of SNS activation on cerebral perfusion, as the ICA is a key supplier of blood to the brain. NEW & NOTEWORTHY We explored the effect of acute sympathetic nervous system (SNS) activation on shear-mediated dilation in the common and internal carotid arteries (CCA and ICA, respectively) in young healthy men. Our data demonstrate that hypercapnia-induced vasodilation of the ICA is attenuated during lower body negative pressure to a greater extent than the CCA. These data may provide novel information related to the role of SNS activation on cerebral perfusion in humans.

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 The cerebrovascular response to lower-body negative pressure vs. head-up tilt

2017 ◽  
Vol 122 (4) ◽  
pp. 877-883 ◽  
Author(s):  
Anne-Sophie G. T. Bronzwaer ◽  
Jasper Verbree ◽  
Wim J. Stok ◽  
Mat J. A. P. Daemen ◽  
Mark A. van Buchem ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Negative Pressure ◽  
Cerebral Blood Flow Velocity ◽  
Lower Body Negative Pressure ◽  
Orthostatic Stress ◽  
Lower Body ◽  
Head Up Tilt ◽  
End Tidal ◽  
Pronounced Reduction

Lower-body negative pressure (LBNP) has been proposed as a MRI-compatible surrogate for orthostatic stress. Although the effects of LBNP on cerebral hemodynamic behavior have been considered to reflect those of orthostatic stress, a direct comparison with actual orthostasis is lacking. We assessed the effects of LBNP (−50 mmHg) vs. head-up tilt (HUT; at 70°) in 10 healthy subjects (5 female) on transcranial Doppler-determined cerebral blood flow velocity (CBF v) in the middle cerebral artery and cerebral perfusion pressure (CPP) as estimated from the blood pressure signal (finger plethysmography). CPP was maintained during LBNP but decreased after 2 min in response to HUT, leading to an ~15% difference in CPP between LBNP and HUT ( P ≤ 0.020). Mean CBF v initially decreased similarly in response to LBNP and for HUT, but, from minute 3 on, the decline became ~50% smaller ( P ≤ 0.029) during LBNP. The reduction in end-tidal Pco2 partial pressure (PetCO2) was comparable but with an earlier return toward baseline values in response to LBNP but not during HUT ( P = 0.008). We consider the larger decrease in CBF v during HUT vs. LBNP attributable to the pronounced reduction in PetCO2 and to gravitational influences on CPP, and this should be taken into account when applying LBNP as an MRI-compatible orthostatic stress modality. NEW & NOTEWORTHY Lower-body negative pressure (LBNP) has the potential to serve as a MRI-compatible surrogate of orthostatic stress but a comparison with actual orthostasis was lacking. This study showed that the pronounced reduction in end-tidal Pco2 together with gravitational effects on the brain circulation lead to a larger decline in cerebral blood flow velocity in response to head-up tilt than during lower-body negative pressure. This should be taken into account when employing lower-body negative pressure as MRI-compatible alternative to orthostatic stress.

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 A Comparison of Protocols for Simulating Hemorrhage in Humans: Step vs. Ramp Lower Body Negative Pressure

2020 ◽  
Author(s):  
Alexander J. Rosenberg ◽  
Victoria L. Kay ◽  
Garen K. Anderson ◽  
Justin D. Sprick ◽  
Caroline A. Rickards
Keyword(s):  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Human Subjects ◽  
Cardiovascular Responses ◽  
Pressure Profile ◽  
Stress Index ◽  
Chamber Pressure ◽  
Lower Body ◽  
Hemodynamic Responses ◽  
Healthy Human

Lower body negative pressure (LBNP) elicits central hypovolemia, and has been used to simulate the cardiovascular and cerebrovascular responses to hemorrhage in humans. LBNP protocols commonly employ progressive stepwise reductions in chamber pressure for specific time periods. However, continuous ramp LBNP protocols have also been utilized to simulate the continuous nature of most bleeding injuries. The aim of this study was to compare tolerance and hemodynamic responses between these two LBNP profiles. Healthy human subjects (N=19; age, 27±4 y; 7F/12M) completed a 1) step LBNP protocol (5-min steps), and; 2) continuous ramp LBNP protocol (3 mmHg/min), both to presyncope. Heart rate (HR), mean arterial pressure (MAP), stroke volume (SV), middle and posterior cerebral artery velocity (MCAv and PCAv), cerebral oxygen saturation (ScO2), and end-tidal CO2 (etCO2) were measured. LBNP tolerance, via the cumulative stress index (CSI, summation of chamber pressure*time at each pressure), and hemodynamic responses were compared between the two protocols. The CSI (Step: 911±97 mmHg*min vs. Ramp: 823±83 mmHg*min; P=0.12) and the magnitude of central hypovolemia (%Δ SV, Step: -54.6±2.6 % vs. Ramp: -52.1±2.8 %; P=0.32) were similar between protocols. While there were no differences between protocols for the maximal %Δ HR (P=0.88), the %Δ MAP during the step protocol was attenuated (P=0.05), and the reductions in MCAv, PCAv, ScO2, and etCO2 were greater (P≤0.08) when compared with the ramp protocol at presyncope. These results indicate that when comparing cardiovascular responses to LBNP across different laboratories, the specific pressure profile must be considered as a potential confounding factor.

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