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

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.

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Pulling back on the push–pull effect: use of lower body negative pressure to protect against drops in cerebral perfusion during airflight manoeuvres

The Journal of Physiology ◽

10.1113/jp280150 ◽

2020 ◽

Vol 598 (15) ◽

pp. 3063-3064

Author(s):

Baraa K. Al‐Khazraji

Keyword(s):

Negative Pressure ◽

Cerebral Perfusion ◽

Lower Body Negative Pressure ◽

Lower Body

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Bloodflow measurements of the neuromuscular apparatus of the internal carotid arteries made by a photometric method. Communication II. Control of the sympathetic nervous system

Bulletin of Experimental Biology and Medicine ◽

10.1007/bf00798813 ◽

1964 ◽

Vol 55 (2) ◽

pp. 128-132

Author(s):

G. I. Mchedlishvili ◽

T. Garbulinskii ◽

A. Gosk

Keyword(s):

Nervous System ◽

Sympathetic Nervous System ◽

Carotid Arteries ◽

Internal Carotid ◽

Photometric Method ◽

Neuromuscular Apparatus ◽

Sympathetic Nervous ◽

Internal Carotid Arteries

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What Is the Role of the Maternal Ophthalmic and Cervical Internal Carotid Arteries in Predicting Maternal Adverse Outcomes in Preeclampsia?

Journal of Ultrasound in Medicine ◽

10.1002/jum.15241 ◽

2020 ◽

Vol 39 (8) ◽

pp. 1527-1535

Author(s):

Mucize Eric Ozdemir ◽

Oya Demirci ◽

Hatice Akay Ozturkmen ◽

Nuray Bakal Ulusoy ◽

Karolin Ohanoglu ◽

...

Keyword(s):

Carotid Arteries ◽

Internal Carotid ◽

Adverse Outcomes ◽

Internal Carotid Arteries

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Change in phase relationship between SBP and R-R interval during lower body negative pressure

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1995.268.4.h1688 ◽

1995 ◽

Vol 268 (4) ◽

pp. H1688-H1693 ◽

Cited By ~ 13

Author(s):

A. P. Blaber ◽

Y. Yamamoto ◽

R. L. Hughson

Keyword(s):

Blood Pressure ◽

Negative Pressure ◽

Time Series Data ◽

Lower Body Negative Pressure ◽

Phase Relationship ◽

Interval Data ◽

Series Data ◽

Lower Body ◽

Healthy Men ◽

Spontaneous Baroreflex

We have investigated the hypothesis that beat-by-beat interaction of systolic blood pressure (SBP) to R-R interval (the spontaneous baroreflex) is dependent on the length of the R-R interval. Data were collected from eight healthy men while heart rate was slow (R-R interval 1,043 +/- 34 ms) and accelerated (R-R interval 804 +/- 18 ms) by application of lower body negative pressure (LBNP greater than or equal to -40 mmHg). Time series data of SBP and R-R interval were searched for spontaneous baroreflex sequences in which R-R interval changed in the same (lag 0), next (lag 1), or next following (lag 2) beat as SBP. This phase relationship was also quantified by cross-spectral analysis. At rest, 85% of all spontaneous baroreflex sequences occurred with no lag (lag 0). With LBNP, there was a significant reduction in the number of lag 0 sequences (26%), whereas lag 1 and lag 2 sequences increased (10–26% and 5–29%, respectively). Cross-spectral phase also changed significantly from -2.3 +/- 6.3 degrees at rest to 70.5 +/- 7.4 degrees during LBNP. These data supported the hypothesis that the lag of a baroreflex event was dependent on the prevailing R-R interval.

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

Journal of Applied Physiology ◽

10.1152/japplphysiol.00623.2018 ◽

2018 ◽

Vol 125 (6) ◽

pp. 1779-1786 ◽

Cited By ~ 7

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.

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Possible role of prostaglandins A1 and B1 in spasm of the internal carotid arteries

Bulletin of Experimental Biology and Medicine ◽

10.1007/bf00798872 ◽

1977 ◽

Vol 83 (6) ◽

pp. 783-785

Author(s):

G. I. Mchedlishvili ◽

L. G. Ormotsadze

Keyword(s):

Carotid Arteries ◽

Internal Carotid ◽

Internal Carotid Arteries

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

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00052.2013 ◽

2013 ◽

Vol 305 (6) ◽

pp. R604-R609 ◽

Cited By ~ 18

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.

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