Electrical activation of the human vestibulo-sympathetic reflex

Voustianiouk, Andrei; Kaufmann, Horacio; Diedrich, André; Raphan, Theodore; Biaggioni, Italo; MacDougall, Hamish G.; Ogorodnikov, Dmitri; Cohen, Bernard

doi:10.1007/s00221-005-0266-9

Cited by 62 publications

(52 citation statements)

References 27 publications

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“…VSR in humans has been found to be a mediator of cardiovascular stress (Dyckman et al 2007, Saunder et al 2008 and to even have shorter response latency than the baroreflex (Kaufman et al 2002 andVoustianiouk et al 2006). The latter finding indicates that the VSR could be the first line-of-defense to cardiovascular stress and thus could play a vital role in maintaining astronaut orthostatic tolerance.…”

Section: Vestibular Motivations For Artificial Gravitymentioning

confidence: 99%

A critical benefit analysis of artificial gravity as a microgravity countermeasure

2010

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Human physiological systems, especially the cardiovascular and musculo-skeletal systems, are well-known to decondition during spaceflight. Several countermeasures that are in use today have been rigorously developed over the decades to combat this deconditioning. However, these countermeasures are system specific and have proven to be only partially effective. Artificial gravity has been persistently discussed as a countermeasure that potentially has salutary effects on all physiological systems, though few ground-based studies have been performed in comparison to other countermeasures. The current analysis attempts to elucidate the effectiveness of artificial gravity by directly comparing results of previously published and unpublished deconditioning studies with those of more traditional, ground-based countermeasures (i.e. resistive exercise, aerobic exercise, lower body negative pressure, or some variation of these). Animal studies were also evaluated to supplement the knowledge base and to fill gaps in the human countermeasure literature. Designs of published studies, such as study duration, deconditioning paradigm, subject selection criteria, measurements taken, etc., were confounding variables; however, studies that had some measure of consistency between these variables were compared, although notable differences were cited in the analysis and discussion. Results indicate that for prolonged spaceflight an artificial gravity-based countermeasure may provide benefits equivalent to traditional countermeasures for the cardiovascular system. Too few comparable, human studies have been performed to draw any conclusions for the musculoskeletal system, although animal studies show some positive results. Gaps in the current knowledge of artificial gravity are identified and guidance for future deconditioning studies is offered. Based on the results of this study, a comprehensive artificial gravity protocol is proposed and future research topics using this countermeasure are

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Section: Vestibular Motivations For Artificial Gravitymentioning

confidence: 99%

A critical benefit analysis of artificial gravity as a microgravity countermeasure

2010

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“…Arterial baroreceptor mechanisms play an important role in regulating peripheral vasoconstriction during postural alterations (23). In addition, there is considerable evidence from studies in animals (6,8,10,11,21,22,32) and humans (1,4,12,23,26,28,30) that the vestibular system also participates in triggering increases in vasomotor activity during movements that promote peripheral blood pooling.Experiments conducted on anesthetized (13, 15) and conscious (32) cats demonstrated that the vestibular system influences on different vascular beds are not equivalent. Electrical stimulation of vestibular afferents produces opposite changes in the activity of sympathetic nerve fibers innervating arterioles in skeletal muscle of the upper and lower body (15) and reciprocal changes in forelimb and hindlimb blood flow (13).…”

mentioning

confidence: 99%

Effects of postural changes and removal of vestibular inputs on blood flow to and from the hindlimb of conscious felines

Yavorcik¹,

Reighard²,

Misra³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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September 30, 2009; doi:10.1152 doi:10. /ajpregu.00551.2009 show that the vestibular system contributes to blood pressure regulation. Prior studies reported that lesions that eliminate inputs from the inner ears attenuate the vasoconstriction that ordinarily occurs in the hindlimbs of conscious cats during head-up rotations. These data led to the hypothesis that labyrinthine-deficient animals would experience considerable lower body blood pooling during head-up postural alterations. The present study tested this hypothesis by comparing blood flow though the femoral artery and vein of conscious cats during 20 -60°head-up tilts from the prone position before and after removal of vestibular inputs. In vestibular-intact animals, venous return from the hindlimb dropped considerably at the onset of head-up tilts and, at 5 s after the initiation of 60°rotations, was 66% lower than when the animals were prone. However, after the animals were maintained in the head-up position for another 15 s, venous return was just 33% lower than before the tilt commenced. At the same time point, arterial inflow to the limb had decreased 32% from baseline, such that the decrease in blood flow out of the limb due to the force of gravity was precisely matched by a reduction in blood reaching the limb. After vestibular lesions, the decline in femoral artery blood flow that ordinarily occurs during head-up tilts was attenuated, such that more blood flowed into the leg. Contrary to expectations, in most animals, venous return was facilitated, such that no more blood accumulated in the hindlimb than when labyrinthine signals were present. These data show that peripheral blood pooling is unlikely to account for the fluctuations in blood pressure that can occur during postural changes of animals lacking inputs from the inner ear. Instead, alterations in total peripheral resistance following vestibular dysfunction could affect the regulation of blood pressure.blood flow patterning; venous return; cardiac output; orthostatic hypotension HEAD-UP BODY ROTATIONS in humans or animals typically result in some pooling of blood in the periphery and a resulting reduction in return of blood to the heart. Because cardiac output is directly related to cardiac preload (Starling's law of the heart) (27), cardiac output tends to decrease during head-up movements (25). Furthermore, cardiac output and peripheral vascular resistance determine systemic blood pressure, such that the sympathetic nervous system must produce a rapid net increase in peripheral resistance by inducing vasoconstriction at the onset of head-up body rotations to maintain stable blood pressure (7). Arterial baroreceptor mechanisms play an important role in regulating peripheral vasoconstriction during postural alterations (23). In addition, there is considerable evidence from studies in animals (6,8,10,11,21,22,32) and humans (1,4,12,23,26,28,30) that the vestibular system also participates in triggering increases in vasomotor activity during movements that promote peripheral blood pooling...

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“…In humans, using head-down rotation (HDR) as a model to activate the vestibular otolith organs, we have demonstrated marked increases in MSNA and peripheral vasoconstriction (15,31,[33][34][35]43). Other studies have supported the presence of the VSR in humans (1,12,19,46). Studies examining changes to the vestibular system after BR are sparse.…”

mentioning

confidence: 96%

Effects of short-term and prolonged bed rest on the vestibulosympathetic reflex

Dyckman

Sauder

Ray

2012

American Journal of Physiology-Heart and Circulatory Physiology

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Dyckman DJ, Sauder CL, Ray CA. Effects of short-term and prolonged bed rest on the vestibulosympathetic reflex. Am J Physiol Heart Circ Physiol 302: H368 -H374, 2012. First published October 21, 2011 doi:10.1152/ajpheart.00193.2011.-The mechanism(s) for post-bed rest (BR) orthostatic intolerance is equivocal. The vestibulosympathetic reflex contributes to postural blood pressure regulation. It was hypothesized that muscle sympathetic nerve responses to otolith stimulation would be attenuated by prolonged head-down BR. Arterial blood pressure, heart rate, muscle sympathetic nerve activity (MSNA), and peripheral vascular conductance were measured during head-down rotation (HDR; otolith organ stimulation) in the prone posture before and after short-duration (24 h; n ϭ 22) and prolonged (36 Ϯ 1 day; n ϭ 8) BR. Head-up tilt at 80°was performed to assess orthostatic tolerance. After short-duration BR, MSNA responses to HDR were preserved (⌬5 Ϯ 1 bursts/min, ⌬53 Ϯ 13% burst frequency, ⌬65 Ϯ 13% total activity; P Ͻ 0.001). After prolonged BR, MSNA responses to HDR were attenuated ϳ50%. MSNA increased by ⌬8 Ϯ 2 vs. ⌬3 Ϯ 2 bursts/min and ⌬83 Ϯ 12 vs. ⌬34 Ϯ 22% total activity during HDR before and after prolonged BR, respectively. Moreover, these results were observed in three subjects tested again after 75 Ϯ 1 days of BR. This reduction in MSNA responses to otolith organ stimulation at 5 wk occurred with reductions in head-up tilt duration. These results indicate that prolonged BR (ϳ5 wk) unlike short-term BR (24 h) attenuates the vestibulosympathetic reflex and possibly contributes to orthostatic intolerance following BR in humans. These results suggest a novel mechanism in the development of orthostatic intolerance in humans. blood pressure; autonomic nervous system; muscle sympathetic nerve activity; hypotension ORTHOSTATIC INTOLERANCE (OI) is the inability to maintain blood pressure and cerebral perfusion while in the upright position. Moreover, the failure to maintain blood pressure in the upright posture is associated with increased mortality (26). Head-down bed rest (BR) is used to simulate microgravity and physical deconditioning and to elicit OI (13). Mechanisms believed to contribute to the development of OI with BR include: impaired vagal baroreflex responses (5), an inadequate increase in sympathetic discharge (18, 42), cardiac atrophy (24), an inability to increase peripheral vascular resistance (3, 25), and hypovolemia (29). Studies indicate that alterations in sympathetic nerve activity contribute to the development of OI (13,18,25,42). Hypotensive episodes during head-up tilt appear to be closely related to lack of increased muscle sympathetic nerve activity (MSNA) (25). MSNA is attenuated during tilt following 14 days of BR in subjects that experienced OI (42). Despite considerable research on this topic, the mechanisms for OI have been an enigma. One possible mechanism for the development of OI after BR that has not been examined is an alteration of the vestibulosympathetic reflex (VSR).Data exist demon...

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Electrical activation of the human vestibulo-sympathetic reflex

Cited by 62 publications

References 27 publications

A critical benefit analysis of artificial gravity as a microgravity countermeasure

A critical benefit analysis of artificial gravity as a microgravity countermeasure

Effects of postural changes and removal of vestibular inputs on blood flow to and from the hindlimb of conscious felines

Effects of short-term and prolonged bed rest on the vestibulosympathetic reflex

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