scholarly journals Forehead versus forearm skin vascular responses at presyncope in humans

2014 ◽  
Vol 307 (7) ◽  
pp. R908-R913 ◽  
Author(s):  
Daniel Gagnon ◽  
R. Matthew Brothers ◽  
Matthew S. Ganio ◽  
Jeffrey L. Hastings ◽  
Craig G. Crandall
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Heat Stress ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Facial Skin ◽  
Vascular Responses ◽  
Radial Artery Catheterization ◽  
Forearm Skin ◽  
Cutaneous Vasoconstriction

Facial pallor is commonly observed at presyncope in humans, suggestive of reductions in facial skin blood flow (SkBF). Yet, cutaneous vasoconstriction is usually minimal at presyncope when measured at the forearm. We tested the hypothesis that reductions in forehead SkBF at presyncope are greater than in the forearm. Forehead and forearm SkBF (laser-Doppler) and blood pressure (Finometer or radial artery catheterization) were measured during lower body negative pressure (LBNP) to presyncope in 11 normothermic and 13 heat-stressed subjects (intestinal temperature increased ∼1.4°C). LBNP reduced mean arterial pressure from 91 ± 5 to 57 ± 7 mmHg during normothermia ( P ≤ 0.001) and from 82 ± 5 to 57 ± 7 mmHg during heat stress ( P ≤ 0.001). During normothermia, LBNP decreased forehead SkBF 55 ± 14% compared with 24 ± 11% at the forearm ( P = 0.002), while during heat stress LBNP decreased forehead SkBF 39 ± 11% compared with 28 ± 8% in the forearm ( P = 0.007). In both conditions, most (≥68%) of the decreases in SkBF were due to decreases in blood pressure. However, a greater contribution of actively mediated reductions in SkBF was observed at the forehead, relative to the forearm during normothermia (32 ± 13% vs. 11 ± 11%, P = 0.031) and heat stress (30 ± 13% vs. 10 ± 13%, P = 0.004). These data suggest that facial pallor at presyncope is due to a combination of passive decreases in forehead SkBF secondary to reductions in blood pressure and to active decreases in SkBF, the latter of which are relatively greater than in the forearm.

scholarly journals Insufficient cutaneous vasoconstriction leading up to and during syncopal symptoms in the heat stressed human

2010 ◽  
Vol 299 (4) ◽  
pp. H1168-H1173 ◽  
Author(s):  
C. G. Crandall ◽  
M. Shibasaki ◽  
T. E. Wilson
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Internal Temperature ◽  
Orthostatic Challenge ◽  
Head Up Tilt ◽  
Cutaneous Vasoconstriction

As much as 50% of cardiac output can be distributed to the skin in the hyperthermic human, and therefore the control of cutaneous vascular conductance (CVC) becomes critical for the maintenance of blood pressure. Little is known regarding the magnitude of cutaneous vasoconstriction in profoundly hypotensive individuals while heat stressed. This project investigated the hypothesis that leading up to and during syncopal symptoms associated with combined heat and orthostatic stress, reductions in CVC are inadequate to prevent syncope. Using a retrospective study design, we evaluated data from subjects who experienced syncopal symptoms during lower body negative pressure ( N = 41) and head-up tilt ( N = 5). Subjects were instrumented for measures of internal temperature, forearm skin blood flow, arterial pressure, and heart rate. CVC was calculated as skin blood flow/mean arterial pressure × 100. Data were obtained while subjects were normothermic, immediately before an orthostatic challenge while heat stressed, and at 5-s averages for the 2 min preceding the cessation of the orthostatic challenge due to syncopal symptoms. Whole body heat stress increased internal temperature (1.25 ± 0.3°C; P < 0.001) and CVC (29 ± 20 to 160 ± 58 CVC units; P < 0.001) without altering mean arterial pressure (83 ± 7 to 82 ± 6 mmHg). Mean arterial pressure was reduced to 57 ± 9 mmHg ( P < 0.001) immediately before the termination of the orthostatic challenge. At test termination, CVC decreased to 138 ± 61 CVC units ( P < 0.001) relative to before the orthostatic challenge but remained approximately fourfold greater than when subjects were normothermic. This negligible reduction in CVC during pronounced hypotension likely contributes to reduced orthostatic tolerance in heat-stressed humans. Given that lower body negative pressure and head-up tilt are models of acute hemorrhage, these findings have important implications with respect to mechanisms of compromised blood pressure control in the hemorrhagic individual who is also hyperthermic (e.g., military personnel, firefighters, etc.).

scholarly journals Validity of auscultatory and Penaz blood pressure measurements during profound heat stress alone and with an orthostatic challenge

2011 ◽  
Vol 301 (5) ◽  
pp. R1510-R1516 ◽  
Author(s):  
Matthew S. Ganio ◽  
R. Matthew Brothers ◽  
Rebekah A. I. Lucas ◽  
Jeffrey L. Hastings ◽  
Craig G. Crandall
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Heat Stress ◽  
Brachial Artery ◽  
Lower Body Negative Pressure ◽  
Peripheral Resistance ◽  
Pressure Measurements ◽  
Lower Body ◽  
Dynamic Changes ◽  
Orthostatic Challenge

Despite frequent reporting of blood pressure (BP) during profound passive heat stress, both with and without a hypotensive challenge, the method by which BP is measured often varies between laboratories. It is unknown whether auscultatory and finger BP measures accurately reflect intra-arterial BP during dynamic changes in cardiac output and peripheral resistance associated with the aforementioned conditions. The purpose of this investigation was to test the hypothesis that auscultatory BP measured at the brachial artery, and finger BP measured by the Penaz method, are valid measures of intra-arterial BP during a passive heat stress and a heat-stressed orthostatic challenge, via lower body negative pressure (LBNP). Absolute (specific aim 1) and the change in (specific aim 2) systolic (SBP), diastolic (DBP), and mean BPs (MBP) were compared at normothermia, after a core temperature increase of 1.47 ± 0.09°C, and during subsequent LBNP. Heat stress did not change auscultatory SBP (6 ± 11 mmHg; P = 0.16), but Penaz SBP (−22 ± 16 mmHg; P < 0.001) and intra-arterial SBP (−11 ± 13 mmHg P = 0.017) decreased. In contrast, DBP and MBP did not differ between methods throughout heat stress. Compared with BP before LBNP, the magnitude of the reduction in BP with all three methods was similar throughout LBNP ( P > 0.05). In conclusion, auscultatory SBP and Penaz SBP failed to track the decrease in intra-arterial SBP that occurred during the profound heat stress, while decreases in arterial BP during an orthostatic challenge are comparable between methodologies.

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 Coronary blood flow responses to physiological stress in humans

2009 ◽  
Vol 296 (3) ◽  
pp. H854-H861 ◽  
Author(s):  
Afsana Momen ◽  
Vernon Mascarenhas ◽  
Amir Gahremanpour ◽  
Zhaohui Gao ◽  
Raman Moradkhan ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Negative Pressure ◽  
Physiological Stress ◽  
Lower Body Negative Pressure ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Lower Body ◽  
Coronary Vasodilation ◽  
Coronary Vasoconstriction

Animal reports suggest that reflex activation of cardiac sympathetic nerves can evoke coronary vasoconstriction. Conversely, physiological stress may induce coronary vasodilation to meet an increased metabolic demand. Whether the sympathetic nervous system can modulate coronary vasomotor tone in response to stress in humans is unclear. Coronary blood velocity (CBV), an index of coronary blood flow, can be measured in humans by noninvasive duplex ultrasound. We studied 11 healthy volunteers and measured beat-by-beat changes in CBV, blood pressure, and heart rate during 1) static handgrip for 20 s at 10% and 70% of maximal voluntary contraction; 2) lower body negative pressure at −10 and −30 mmHg for 3 min each; 3) cold pressor test for 90 s; and 4) hypoxia (10% O2), hyperoxia (100% O2), and hypercapnia (5% CO2) for 5 min each. At the higher level of handgrip, mean blood pressure increased ( P < 0.001), whereas CBV did not change [ P = not significant (NS)]. In addition, during lower body negative pressure, CBV decreased ( P < 0.02; and P < 0.01, for −10 and −30 mmHg, respectively), whereas blood pressure did not change ( P = NS). The dissociation between the responses of CBV and blood pressure to handgrip and lower body negative pressure is consistent with coronary vasoconstriction. During hypoxia, CBV increased ( P < 0.02) and decreased during hyperoxia ( P < 0.01), although blood pressure did not change ( P = NS), suggesting coronary vasodilation during hypoxia and vasoconstriction during hyperoxia. In contrast, concordant increases in CBV and blood pressure were noted during the cold pressor test, and hypercapnia had no effects on either parameter. Thus the physiological stress known to be associated with sympathetic activation can produce coronary vasoconstriction in humans. Contrasting responses were noted during systemic hypoxia and hyperoxia where mechanisms independent of autonomic influences appear to dominate the vascular end-organ effects.

Angiotensin II augments sympathetically mediated arteriolar constriction in man

1991 ◽  
Vol 81 (2) ◽  
pp. 261-266 ◽  
Author(s):  
Peter H. Seidelin ◽  
Joseph G. Collier ◽  
Allan D. Struthers ◽  
David J. Webb
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Negative Pressure ◽  
Animal Studies ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Resistance Vessels ◽  
Sympathetic Vasoconstriction ◽  
Adrenergic Neurotransmission

1. In animal studies, angiotensin II facilitates adrenergic neurotransmission by both pre- and postsynaptic mechanisms. We have investigated whether this interaction occurs in forearm resistance vessels in man. 2. The effect of arterial infusion of angiotensin II (320 fmol/min) on sympathetic vasoconstriction produced by lower-body negative pressure (15 mmHg) was studied in six subjects, and that on the response to exogenous noradrenaline (37.5–150 pmol/min) was studied in a further eight subjects. Forearm blood flow was measured by strain-gauge plethysmography. 3. The dose of angiotensin II was chosen to produce no alteration in resting blood flow, and those of noradrenaline were selected to provide a reduction in blood flow equivalent to that produced by lower-body negative pressure. 4. Lower-body negative pressure produced no change in heart rate or diastolic blood pressure, but caused an initial 5 mmHg fall in systolic blood pressure (P < 0.01). Blood flow was reduced by 21 ± 6% in both forearms by lower-body negative pressure during saline infusion. During angiotensin II infusion, there was a marked difference in the response to lower-body negative pressure, with blood flow being reduced by 40 ± 7% in the infused arm, but only by 21 ± 4% in the control arm (P < 0.05). Angiotensin II infusion had no effect on resting blood flow or the responses to noradrenaline. 5. We conclude that angiotensin II augments sympathetic vasoconstriction in forearm resistance vessels in man at a concentration that has no direct effect on blood flow. The absence of an effect of angiotensin II on the response to noradrenaline suggests that augmentation of sympathetic vasoconstriction occurs pre-synaptically through facilitation of noradrenaline release.

Forearm skin and muscle vasoconstriction during lower body negative pressure

1986 ◽  
Vol 60 (5) ◽  
pp. 1535-1541 ◽  
Author(s):  
A. Tripathi ◽  
E. R. Nadel
Keyword(s):  
Blood Flow ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Venous Occlusion ◽  
Lower Body ◽  
Total Blood ◽  
Forearm Skin ◽  
The Difference ◽  
Total Blood Flow ◽  
Male Subjects

In view of conflicting reports of skeletal muscle and skin blood flow participation in baroreceptor-mediated reflexes, we studied the effects of graded lower body negative pressure (LBNP) on cutaneous and muscular components of forearm blood flow (FBF) in seven male subjects at 28 degrees C. FBF was measured by venous occlusion plethysmography and cutaneous flow by laser-Doppler velocimetry, the difference being the muscular flow. Mean FBF decreased by 39 and 56% from control at LBNP of 20 and 50 Torr, respectively. Skin flow decreased linearly with graded LBNP contributing 32% of the decrease of total blood flow at 20 Torr and then 50% of total decrease of blood flow at 50 Torr. Conversely, the decrease in muscle flow represented 68% of the total decrease at LBNP of 20 Torr and then 50% of the total decrease at LBNP of 50 Torr. We concluded that both skin and muscle circulations participate in sustained peripheral vasoconstriction during LBNP, with muscle flow achieving near maximum vasoconstriction by 20 Torr and skin showing a graded vasoconstriction to decreases in LBNP.

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.

scholarly journals Combined heat and mental stress alters neurovascular control in humans

2010 ◽  
Vol 109 (6) ◽  
pp. 1880-1886 ◽  
Author(s):  
Jenna C. Klein ◽  
Craig G. Crandall ◽  
R. Matthew Brothers ◽  
Jason R. Carter
Keyword(s):  
Heart Rate ◽  
Heat Stress ◽  
Mental Stress ◽  
Muscle Sympathetic Nerve Activity ◽  
Thermal Conditions ◽  
Venous Occlusion ◽  
Vascular Conductance ◽  
Vascular Responses ◽  
Time Condition ◽  
Forearm Skin

This study examined the effect of combined heat and mental stress on neurovascular control. We hypothesized that muscle sympathetic nerve activity (MSNA) and forearm vascular responses to mental stress would be augmented during heat stress. Thirteen subjects performed 5 min of mental stress during normothermia (Tcore; 37 ± 0°C) and heat stress (38 ± 0°C). Heart rate, mean arterial pressure (MAP), MSNA, forearm vascular conductance (FVC; venous occlusion plethysmography), and forearm skin vascular conductance (SkVCf; via laser-Doppler) were analyzed. Heat stress increased heart rate, MSNA, SkVCf, and FVC at rest but did not change MAP. Mental stress increased MSNA and MAP during both thermal conditions; however, the increase in MAP during heat stress was blunted, whereas the increase in MSNA was accentuated, compared with normothermia (time × condition; P < 0.05 for both). Mental stress decreased SkVCf during heat stress but not during normothermia (time × condition, P < 0.01). Mental stress elicited similar increases in heart rate and FVC during both conditions. In one subject combined heat and mental stress induced presyncope coupled with atypical blood pressure and cutaneous vascular responses. In conclusion, these findings indicate that mental stress elicits a blunted increase of MAP during heat stress, despite greater increases in total MSNA and cutaneous vasoconstriction. The neurovascular responses to combined heat and mental stress may be clinically relevant to individuals frequently exposed to mentally demanding tasks in hyperthermic environmental conditions (i.e., soldiers, firefighters, and athletes).

Clinical Efficacy of EH0202, a Kampo Formula, on the Health of Middle-Aged Women

2004 ◽  
Vol 32 (05) ◽  
pp. 755-770 ◽  
Author(s):  
Takahisa Ushiroyama ◽  
Satoshi Yoshida ◽  
Keiichi Tadaki ◽  
Atsushi Ikeda ◽  
Minoru Ueki
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Plasma Lipid ◽  
Skin Surface ◽  
Menopausal Symptoms ◽  
Clinical Effects ◽  
Facial Skin ◽  
Herbal Supplement ◽  
Menopausal Women ◽  
Post Menopausal

To investigate the clinical effects of EH0202, a Japanese herbal supplement, on the menopausal symptoms and physical status of peri- and post-menopausal women. Thirty-two post-menopausal women (53.0±5.1 years) presented with menopausal complaints were enrolled in the clinical study. Patients were administered an herbal supplement, EH0202 (6 g/day for 6 months), and were assessed for improvement of their overall symptoms using the Greene Climacteric Scale and the Visual Analog Scale (VAS). Blood pressure, skin surface blood flow and plasma lipid profiles were measured before and 1, 3 and 6 months after EH0202 administration. There was a significant decrease in the climacteric scale score (P<0.001) and VAS (P<0.0001) after 6 months of EH0202 treatment. There was a significant decrease in systolic (P<0.001) and diastolic (P<0.05) blood pressure, and a significant decrease in facial skin surface blood flow (P<0.05) after 3 months of EH0202 administration. We observed a significant decrease in plasma TG and LDL-cholesterol concentrations after 3 months of EH0202 administration (P<0.05). EH0202 (MACH) reduced blood pressure, excess facial skin blood flow (flushing) and abnormal lipid levels, as well as clinically improved menopausal symptoms in post-menopausal women. In post-menopausal women, this product appears to help maintain normal biological function and improves quality of life.

Noise-Enhanced Heart Rate and Sympathetic Nerve Responses to Oscillatory Lower Body Negative Pressure in Humans

2001 ◽  
Vol 86 (2) ◽  
pp. 559-564 ◽  
Author(s):  
Ichiro Hidaka ◽  
Shin-Ichi Ando ◽  
Hideaki Shigematsu ◽  
Koji Sakai ◽  
Soko Setoguchi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Stochastic Resonance ◽  
Negative Pressure ◽  
Sympathetic Nerve ◽  
Carotid Sinus ◽  
Lower Body Negative Pressure ◽  
Arterial System ◽  
Lower Body ◽  
Cardiopulmonary Baroreceptors

By injecting noise into the carotid sinus baroreceptors, we previously showed that heart rate (HR) responses to weak oscillatory tilt were enhanced via a mechanism known as “stochastic resonance.” It remains unclear, however, whether the same responses would be observed when using oscillatory lower body negative pressure (LBNP), which would unload the cardiopulmonary baroreceptors with physically negligible effects on the arterial system. Also, the vasomotor sympathetic activity directly controlling peripheral resistance against hypotensive stimuli was not observed. We therefore investigated the effects of weak (0 to approximately −10 mmHg) oscillatory (0.03 Hz) LBNP on HR and muscle sympathetic nerve activity (MSNA) while adding incremental noise to the carotid sinus baroreceptors via a pneumatic neck chamber. The signal-to-noise ratio of HR, cardiac interbeat interval, and total MSNA were all significantly improved by increasing noise intensity, while there was no significant change in the arterial blood pressure in synchronized with the oscillatory LBNP. We conclude that the stochastic resonance, affecting both HR and MSNA, results from the interaction of noise with the signal in the brain stem, where the neuronal inputs from the arterial and cardiopulmonary baroreceptors first come together in the nucleus tractus solitarius. Also, these results indicate that the noise could induce functional improvement in human blood pressure regulatory system in overcoming given hypotensive stimuli.

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