Vasoconstrictor Reserve and Sympathetic Neural Control of Orthostasis

Fu, Qi; Witkowski, Sarah; Levine, Benjamin D.

doi:10.1161/01.cir.0000146384.91715.b5

Cited by 110 publications

(97 citation statements)

References 53 publications

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“…In the resting, supine posture breathing through the active ITD did not elicit an increase in directly measured muscle sympathetic nerve activity (MSNA), nor was there an increase in mean CBFV LF (12). Application of progressive LBNP and the reduction in central blood volume, however, does elicit increases in both MSNA (7,15,34) and mean CBFV LF (43). Interestingly, in the current study, LBNP alone (sham ITD trial) did not increase CBFV LF , but the combined effect of LBNP and active ITD breathing elevated CBFV LF by 209%.…”

Section: Discussionmentioning

confidence: 98%

Inspiratory resistance delays the reporting of symptoms with central hypovolemia: association with cerebral blood flow

Rickards

Ryan

Cooke

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Rickards CA, Ryan KL, Cooke WH, Lurie KG, Convertino VA. Inspiratory resistance delays the reporting of symptoms with central hypovolemia: association with cerebral blood flow. Am J Physiol Regul Integr Comp Physiol 293: R243-R250, 2007. First published May 16, 2007; doi:10.1152/ajpregu.00087.2007.-We tested the hypothesis that breathing through an inspiratory threshold device (ITD) during progressive central hypovolemia would protect cerebral perfusion and attenuate the reporting of presyncopal symptoms. Eight human subjects were exposed to lower-body negative pressure (LBNP) until the presence of symptoms while breathing through either an active ITD (Ϫ7 cmH2O impedance) or a sham ITD (0 cmH2O). Cerebral blood flow velocity (CBFV) was measured continuously via transcranial Doppler and analyzed in both time and frequency domains. Subjects were asked to report any subjective presyncopal symptoms (e.g., dizziness, nausea) at the conclusion of each LBNP exposure. Symptoms were coincident with physiological evidence of cardiovascular collapse (e.g., hypotension, bradycardia). Breathing on the active ITD increased LBNP tolerance time (mean Ϯ SE) from 2,014 Ϯ 106 s to 2,259 Ϯ 138 s (P ϭ 0.006). We compared CBFV responses at the time of symptoms during the sham ITD trial with those at the same absolute time during the active ITD trial (when there were no symptoms). While there was no difference in mean CBFV at these time points (sham, 44 Ϯ 4 cm/s vs. active, 47 Ϯ 4; P ϭ 0.587), total oscillations (sum of high-and low-frequency spectral power) of CBFV were higher (P ϭ 0.004) with the active ITD (45.6 Ϯ 10.2 cm/s 2 ) than the sham ITD (22.1 Ϯ 5.4 cm/s 2 ). We conclude that greater oscillations around the same absolute level of mean CBFV are induced by inspiratory resistance and may contribute to the delay in symptoms and cardiovascular collapse that accompany progressive central hypovolemia.inspiratory threshold device; cerebral blood flow regulation; lowerbody negative pressure THE PRESERVATION OF CEREBRAL blood flow during hypotensive stress is integral in delaying the onset of presyncopal symptoms and maintaining consciousness. Recent data reported from several investigations have demonstrated the benefits of an inspiratory impedance threshold device (ITD) in elevating cerebral perfusion pressure in animals (39, 40) and reducing the reporting of presyncopal symptoms in humans (8, 27) with reductions in central blood volume.The ITD was designed to create a greater reduction in intrathoracic pressure during inspiration, enhancing the natural vacuum within the chest (26, 37). This vacuum promotes an increase in venous return, thereby increasing ventricular preload and subsequent cardiac output (Q) and arterial blood pressure (9, 26). Breathing on the ITD also increases cerebral blood flow velocity (CBFV) in resting, supine humans (12) and in the hemorrhaging porcine model, application of negative intrathoracic pressure reduces intracranial pressure (ICP) and subsequently elevates cerebral perfusion pressure (40, 41). Th...

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Section: Discussionmentioning

confidence: 98%

Inspiratory resistance delays the reporting of symptoms with central hypovolemia: association with cerebral blood flow

Rickards

Ryan

Cooke

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

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“…Conversely, syncope during sustained orthostasis is reportedly dependant on the neural and vasomotor reserve available for vasoconstriction (Fu et al 2004). Indeed, vasovagal (reflex) syncope is the most prevalent identified cause of fainting and is generated by systemic arterial hypotension, resulting from reflex vasodilation, bradycardia or both (Brignole et al 2004).…”

mentioning

confidence: 99%

Compression leggings modestly affect cardiovascular but not cerebrovascular responses to heat and orthostatic stress in young and older adults

Lucas

Ainslie

Morrison

et al. 2011

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We tested the hypothesis that wearing commercially available compression leggings would attenuate postural reductions in mean arterial blood pressure (MAP) and cerebral perfusion during heat stress, particularly in older adults. Six older (70 years±4) and six younger (29 years±4) males were heated (esophageal temperature raised 0.5°C) in a water-perfused suit whilst wearing compression or control leggings (>1 week apart, randomized order). Blood flow velocity in the middle cerebral artery (MCAv), blood pressure (photoplethysmography), total peripheral resistance (TPR; ModelFlow) and the partial pressure of end-tidal carbon dioxide were measured continuously before and during 3-min standing in each thermal state. When supine, compression leggings did not change any cardiorespiratory variables in either age group or thermal condition (P>0.05). Upon standing, wearing compression leggings delayed (~15%; P=0.044) the maximal drop (nadir) in MAP irrespective of age or thermal condition. During the last minute of standing, wearing compression leggings in normothermia increased TPR (+16%) in older participants but dropped TPR (−8%) in younger participants (P=0.004 compression×age group). When standing and heated, wearing compression leggings lowered TPR in older and younger participants (~43%; P<0.01) without changing MAP or MCAv (P>0.05). In older adults, when standing, compression leggings maintained MAP by elevating TPR. In contrast, under combined heat and orthostatic stress, wearing compression leggings dropped TPR in both older and younger adults, though MAP and MCAv were maintained.

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“…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).…”

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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Vasoconstrictor Reserve and Sympathetic Neural Control of Orthostasis

Cited by 110 publications

References 53 publications

Inspiratory resistance delays the reporting of symptoms with central hypovolemia: association with cerebral blood flow

Inspiratory resistance delays the reporting of symptoms with central hypovolemia: association with cerebral blood flow

Compression leggings modestly affect cardiovascular but not cerebrovascular responses to heat and orthostatic stress in young and older adults

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

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