Circulation and respiration response to arm exercise and lower body negative pressure

Kobayashi, Yoshio; Ja, Loeppky; Venters,; Uc, Luft

doi:10.1249/00005768-198024000-00003

Cited by 2 publications

(2 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the other study, LBNP‐induced decreases in P

_{ET,CO_{2}}

occurred, but were not statistically significant (Serrador et al 2000). In several other previous reports, hyperventilation‐induced hypocapnia was a consistent, statistically significant finding during simulated orthostatic stress with LBNP and also during upright tilt (Kobayashi et al 1980; Ahn et al 1989; Cencetti et al 1997; Cooke et al 1999). In our subjects, we observed a drop in CFV at the onset of LBNP when P ET,CO2 levels were allowed to fall; however, when we restored P

_{ET,CO_{2}}

to control by supplementing the inspired CO 2 , we also restored the control level of CFV (Tables 1 and 2).…”

Section: Discussionsupporting

confidence: 82%

Baroreflex‐induced sympathetic activation does not alter cerebrovascular CO₂ responsiveness in humans

LeMarbre

Stauber

Khayat

et al. 2003

The Journal of Physiology

View full text Add to dashboard Cite

We investigated the effect of baroreflex‐induced sympathetic activation, produced by lower body negative pressure (LBNP) at −40 mmHg, on cerebrovascular responsiveness to hyper‐ and hypocapnia in healthy humans. Transcranial Doppler ultrasound was used to measure blood flow velocity (CFV) in the middle cerebral artery during variations in end‐tidal carbon dioxide pressure (PET,CO2) of +10, +5, 0, −5, and −10 mmHg relative to eupnoea. The slopes of the linear relationships between PET,CO2 and CFV were computed separately for hyper‐ and hypocapnia during the LBNP and no‐LBNP conditions. LBNP decreased pulse pressure, but did not change mean arterial pressure. LBNP evoked an increase in ventilation that resulted in a 9 ± 2 mmHg decrease in PET,CO2, which was corrected by CO2 supplementation of the inspired air. LBNP did not affect cerebrovascular CO2 response slopes during steady‐state hypercapnia (3.14 ± 0.24 vs. 2.96 ± 0.26 cm s−1 mmHg−1) or hypocapnia (1.31 ± 0.18 vs. 1.32 ± 0.19 cm s−1 mmHg−1), or the CFV responses to voluntary apnoea (+51 ± 19 vs.+50 ± 18 %). Thus, cerebrovascular CO2 responsiveness was not altered by baroreflex‐induced sympathetic activation. Our data challenge the concept that sympathetic activation restrains cerebrovascular responses to alterations in CO2 pressure.

show abstract

“…In the other study, LBNP‐induced decreases in P

_{ET,CO_{2}}

_{ET,CO_{2}}

to control by supplementing the inspired CO 2 , we also restored the control level of CFV (Tables 1 and 2).…”

Section: Discussionsupporting

confidence: 82%

Baroreflex‐induced sympathetic activation does not alter cerebrovascular CO₂ responsiveness in humans

LeMarbre

Stauber

Khayat

et al. 2003

The Journal of Physiology

View full text Add to dashboard Cite

show abstract

“…One could argue that there may be dissociation between end-tidal CO 2 and arterial CO 2 during LBP, and thus the former may not accurately reflect the latter. Venous pooling from postural change does impact the arterial to alveolar CO 2 gradient: during negative LBP and head-up tilt, there is a 2 to 4 mmHg difference in arterial to alveolar CO 2 (20), which represents an enlargement in alveolar dead space due to regional underperfusion of the lungs (rather than overventilation) (5,39,42,53). Indeed, the physiological dead space (the portion of expired gas that does not remove CO 2 from the pulmonary blood flow) is increased during standing by~80 ml (37,39).…”

Section: Discussionmentioning

confidence: 99%

Relative contributions of systemic hemodynamic variables to cerebral autoregulation during orthostatic stress

Yoshida

Hamner

Ishibashi

et al. 2018

Journal of Applied Physiology

View full text Add to dashboard Cite

Postural changes impair the ability of the cerebrovasculature to buffer against dynamic pressure fluctuations, but the mechanisms underlying this impairment have not been elucidated. We hypothesized that autoregulatory impairment may reflect the impact of static central volume shifts on hemodynamic factors other than arterial pressure (AP). In 14 young volunteers, we assessed the relation of fluctuations in cerebral blood flow (CBF) to those in AP, cardiac output, and CO, during oscillatory lower body pressure (LBP) (±20 mmHg at 0.01 and 0.06 Hz) at three static levels (-20, 0, and +20 mmHg). Static and dynamic changes in AP, cardiac output, and CO explained over 70% of the variation in CBF fluctuations. However, their contributions were different across frequencies and levels: dynamic AP changes explained a substantial proportion of the variation in faster CBF fluctuations (partial R = 0.75, standardized β = 0.83, P < 0.01), whereas those in CO explained the largest portion of the variation in slow fluctuations (partial R = 0.43, β = 0.51, P < 0.01). There was, however, a major contribution of slow dynamic AP changes during negative (β = 0.43) but not neutral (β = 0.05) or positive (β = -0.07) LBP. This highlights the differences in contributions of systemic variables to dynamic and static autoregulation and has important implications for understanding orthostatic intolerance. NEW & NOTEWORTHY While fluctuations in blood pressure drive faster fluctuations in cerebral blood flow, overall level of CO and the magnitude of its fluctuations, along with cardiac output, determine the magnitude of slow ones. The effect of slow blood pressure fluctuations on cerebrovascular responses becomes apparent only during pronounced central volume shifts (such as when standing). This underlines distinct but interacting contributions of static and dynamic changes in systemic hemodynamic variables to the cerebrovascular regulation.

show abstract

Circulation and respiration response to arm exercise and lower body negative pressure

Cited by 2 publications

References 0 publications

Baroreflex‐induced sympathetic activation does not alter cerebrovascular CO₂ responsiveness in humans

Baroreflex‐induced sympathetic activation does not alter cerebrovascular CO₂ responsiveness in humans

Relative contributions of systemic hemodynamic variables to cerebral autoregulation during orthostatic stress

Contact Info

Product

Resources

About

Circulation and respiration response to arm exercise and lower body negative pressure

Cited by 2 publications

References 0 publications

Baroreflex‐induced sympathetic activation does not alter cerebrovascular CO2 responsiveness in humans

Baroreflex‐induced sympathetic activation does not alter cerebrovascular CO2 responsiveness in humans

Relative contributions of systemic hemodynamic variables to cerebral autoregulation during orthostatic stress

Contact Info

Product

Resources

About

Baroreflex‐induced sympathetic activation does not alter cerebrovascular CO₂ responsiveness in humans

Baroreflex‐induced sympathetic activation does not alter cerebrovascular CO₂ responsiveness in humans