Cerebral blood flow oscillations elicited by inspiratory resistance delays the reporting of orthostatic symptoms with central hypovolemia

Neurovascular coupling (NVC) describes the link between an increase in task-related neural activity and increased cerebral blood flow denoted “functional hyperemia.” We previously showed induced cerebral blood flow oscillations suppressed functional hyperemia; conversely functional hyperemia also suppressed cerebral blood flow oscillations. We used lower body negative pressure (OLBNP) oscillations to force oscillations in middle cerebral artery cerebral blood flow velocity (CBFv). Here, we used N-back testing, an intellectual memory challenge as a neural activation task, to test the hypothesis that OLBNP-induced oscillatory cerebral blood flow can reduce functional hyperemia and NVC produced by a working memory task and can interfere with working memory. We used OLBNP (−30 mmHg) at 0.03, 0.05, and 0.10 Hz and measured spectral power of CBFv at all frequencies. Neither OLBNP nor N-back, alone or combined, affected hemodynamic parameters. 2-Back power and OLBNP individually were compared with 2-back power during OLBNP. 2-Back alone produced a narrow band increase in oscillatory arterial pressure (OAP) and oscillatory cerebral blood flow power centered at 0.0083 Hz. Functional hyperemia in response to 2-back was reduced to near baseline and 2-back memory performance was decreased by 0.03-, 0.05-, and 0.10-Hz OLBNP. OLBNP alone produced increased oscillatory power at frequencies of oscillation not suppressed by added 2-back. However, 2-back preceding OLBNP suppressed OLBNP power. OLBNP-driven oscillatory CBFv blunts NVC and memory performance, while memory task reciprocally interfered with forced CBFv oscillations. This shows that induced cerebral blood flow oscillations suppress functional hyperemia and functional hyperemia suppresses cerebral blood flow oscillations. NEW & NOTEWORTHY We show that induced cerebral blood flow oscillations suppress functional hyperemia produced by a working memory task as well as memory task performance. We conclude that oscillatory cerebral blood flow produces causal reductions of memory task neurovascular coupling and memory task performance. Reductions of functional hyperemia are constrained by autoregulation.

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Oscillatory lower body negative pressure impairs task related functional hyperemia in healthy volunteers

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00747.2015 ◽

2016 ◽

Vol 310 (6) ◽

pp. H775-H784 ◽

Cited By ~ 5

Author(s):

Julian M. Stewart ◽

Keshawadhana Balakrishnan ◽

Paul Visintainer ◽

Andrew T. Del Pozzi ◽

Zachary R. Messer ◽

...

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Healthy Volunteers ◽

Flow Velocity ◽

Negative Pressure ◽

Lower Body Negative Pressure ◽

Lower Body ◽

Functional Hyperemia ◽

Blood Flow Oscillations ◽

Flow Oscillations

Neurovascular coupling refers to the link between an increase in neural activity in response to a task and an increase in cerebral blood flow denoted “functional hyperemia.” Recent work on postural tachycardia syndrome indicated that increased oscillatory cerebral blood flow velocity (CBFv) was associated with reduced functional hyperemia. We hypothesized that a reduction in functional hyperemia could be causally produced in healthy volunteers by using oscillations in lower body negative pressure (OLBNP) to force oscillations in CBFv. CBFv was measured by transcranial Doppler ultrasound of the left middle cerebral artery. We used passive arm flexion applied during eight periodic 60-s flexion/60-s relaxation epochs to produce 120-s periodic changes in functional hyperemia (at 0.0083 Hz). We used −30 mmHg of OLBNP at 0.03, 0.05, and 0.10 Hz, the range for cerebral autoregulation, and measured spectral power of CBFv at all frequencies. Arm flexion power performed without OLBNP was compared with arm flexion power during OLBNP. OLBNP power performed in isolation was compared with power during OLBNP plus arm flexion. Cerebral flow velocity oscillations at 0.05 Hz reduced and at 0.10 Hz eliminated functional hyperemia, while 0.03 Hz did not reach significance. In contrast, arm flexion reduced OLBNP-induced oscillatory power at all frequencies. The interactions between OLBNP-driven CBFv oscillations and arm flexion-driven CBFv oscillations are reciprocal. Thus induced cerebral blood flow oscillations suppress functional hyperemia, and functional hyperemia suppresses cerebral blood flow oscillations. We conclude that oscillatory cerebral blood flow produces a causal reduction of functional hyperemia.

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Sensitivity of the Laser Doppler Flowmetry and Incoherent Optical Flowmetry to Low-frequency Blood Flow Oscillations

2020 International Conference Laser Optics (ICLO) ◽

10.1109/iclo48556.2020.9285553 ◽

2020 ◽

Author(s):

D.G. Lapitan ◽

D.A. Rogatkin

Keyword(s):

Blood Flow ◽

Laser Doppler Flowmetry ◽

Low Frequency ◽

Laser Doppler ◽

Blood Flow Oscillations ◽

Doppler Flowmetry ◽

Flow Oscillations

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Formation of the peak amplitude of blood flow oscillations at a frequency of 0.1 Hz in the human cardiovascular system by the noise effect on the heart

10.1117/12.2267634 ◽

2017 ◽

Cited By ~ 1

Author(s):

Andrey A. Grinevich ◽

Arina V. Tankanag ◽

Nikolay K. Chemeris

Keyword(s):

Blood Flow ◽

Cardiovascular System ◽

Peak Amplitude ◽

Blood Flow Oscillations ◽

Noise Effect ◽

Flow Oscillations ◽

Human Cardiovascular System

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

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00087.2007 ◽

2007 ◽

Vol 293 (1) ◽

pp. R243-R250 ◽

Cited By ~ 40

Author(s):

Caroline A. Rickards ◽

Kathy L. Ryan ◽

William H. Cooke ◽

Keith G. Lurie ◽

Victor A. Convertino

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Cerebral Blood Flow Velocity ◽

Lower Body Negative Pressure ◽

Spectral Power ◽

Human Subjects ◽

Low Frequency ◽

Cardiovascular Collapse ◽

Absolute Level ◽

Inspiratory Resistance

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 (−7 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 ± SE) from 2,014 ± 106 s to 2,259 ± 138 s ( P = 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 ± 4 cm/s vs. active, 47 ± 4; P = 0.587), total oscillations (sum of high- and low-frequency spectral power) of CBFV were higher ( P = 0.004) with the active ITD (45.6 ± 10.2 cm/s2) than the sham ITD (22.1 ± 5.4 cm/s2). 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.

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