scholarly journals Effect of acute hypoxemia on cerebral blood flow velocity control during lower body negative pressure

2018 ◽  
Vol 6 (4) ◽  
pp. e13594 ◽  
Author(s):  
Noud van Helmond ◽  
Blair D. Johnson ◽  
Walter W. Holbein ◽  
Humphrey G. Petersen-Jones ◽  
Ronée E. Harvey ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Flow Velocity ◽  
Negative Pressure ◽  
Blood Flow Velocity ◽  
Cerebral Blood Flow Velocity ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Velocity Control

Cerebral Blood Flow Velocity During Combined Lower Body Negative Pressure and Cognitive Stress

2015 ◽  
Vol 86 (8) ◽  
pp. 688-692 ◽  
Author(s):  
John J. Durocher ◽  
Jason R. Carter ◽  
William H. Cooke ◽  
Angelea H. Young ◽  
Morton H. Harwood
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Flow Velocity ◽  
Negative Pressure ◽  
Blood Flow Velocity ◽  
Cerebral Blood Flow Velocity ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Cognitive Stress

scholarly journals The cerebrovascular response to lower-body negative pressure vs. head-up tilt

2017 ◽  
Vol 122 (4) ◽  
pp. 877-883 ◽  
Author(s):  
Anne-Sophie G. T. Bronzwaer ◽  
Jasper Verbree ◽  
Wim J. Stok ◽  
Mat J. A. P. Daemen ◽  
Mark A. van Buchem ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Negative Pressure ◽  
Cerebral Blood Flow Velocity ◽  
Lower Body Negative Pressure ◽  
Orthostatic Stress ◽  
Lower Body ◽  
Head Up Tilt ◽  
End Tidal ◽  
Pronounced Reduction

Lower-body negative pressure (LBNP) has been proposed as a MRI-compatible surrogate for orthostatic stress. Although the effects of LBNP on cerebral hemodynamic behavior have been considered to reflect those of orthostatic stress, a direct comparison with actual orthostasis is lacking. We assessed the effects of LBNP (−50 mmHg) vs. head-up tilt (HUT; at 70°) in 10 healthy subjects (5 female) on transcranial Doppler-determined cerebral blood flow velocity (CBF v) in the middle cerebral artery and cerebral perfusion pressure (CPP) as estimated from the blood pressure signal (finger plethysmography). CPP was maintained during LBNP but decreased after 2 min in response to HUT, leading to an ~15% difference in CPP between LBNP and HUT ( P ≤ 0.020). Mean CBF v initially decreased similarly in response to LBNP and for HUT, but, from minute 3 on, the decline became ~50% smaller ( P ≤ 0.029) during LBNP. The reduction in end-tidal Pco2 partial pressure (PetCO2) was comparable but with an earlier return toward baseline values in response to LBNP but not during HUT ( P = 0.008). We consider the larger decrease in CBF v during HUT vs. LBNP attributable to the pronounced reduction in PetCO2 and to gravitational influences on CPP, and this should be taken into account when applying LBNP as an MRI-compatible orthostatic stress modality. NEW & NOTEWORTHY Lower-body negative pressure (LBNP) has the potential to serve as a MRI-compatible surrogate of orthostatic stress but a comparison with actual orthostasis was lacking. This study showed that the pronounced reduction in end-tidal Pco2 together with gravitational effects on the brain circulation lead to a larger decline in cerebral blood flow velocity in response to head-up tilt than during lower-body negative pressure. This should be taken into account when employing lower-body negative pressure as MRI-compatible alternative to orthostatic stress.

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

2016 ◽  
Vol 310 (6) ◽  
pp. H775-H784 ◽  
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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