Cardiovascular regulation of bedridden patients with severe physical disabilities to orthostatic stress and lower body negative pressure

1991 ◽  
Vol 3 (1) ◽  
pp. 1-11 ◽  
Author(s):  
K. Mita ◽  
K. Akataki ◽  
N. Suzuki ◽  
T. Miyagawa ◽  
N. Ishida ◽  
...  
1987 ◽  
Vol 63 (2) ◽  
pp. 719-725 ◽  
Author(s):  
C. M. Tomaselli ◽  
M. A. Frey ◽  
R. A. Kenney ◽  
G. W. Hoffler

We have investigated the pattern of fluid redistribution and cardiovascular responses during graduated orthostatic stress. Twelve men, age 30–39 yr, underwent a 25-min lower-body negative pressure (LBNP) test protocol that involved sequential stages of LBNP at -8 mmHg (1 min), -16 mmHg (1 min), -30 mmHg (3 min), -40 mmHg (5 min), -50 mmHg (5 min), -40 mmHg (5 min), -30 mmHg (3 min), -16 mmHg (1 min), and -8 mmHg (1 min). Data were recorded at the end of each stage. For many measured variables values during the descending phase of LBNP (-8 to -40 mmHg) were significantly different from values during the ascending phase of (-40 to -8 mmHg). These differences appear to be due to a component of fluid translocation that occurs during LBNP and cannot be reversed within the duration of the procedure. We hypothesize that this slowly reversed component is sequestration of fluid in the interstitial and lymphatic compartments. In contrast, venous pooling is a rapidly reversible component of fluid movement during LBNP. A scheme describing fluid and cardiovascular responses to LBNP based on these data and the data of other investigators is presented.


1987 ◽  
Vol 63 (6) ◽  
pp. 2558-2562 ◽  
Author(s):  
R. G. Victor ◽  
W. N. Leimbach

Recent studies indicate that nonhypotensive orthostatic stress in humans causes reflex vasoconstriction in the forearm but not in the calf. We used microelectrode recordings of muscle sympathetic nerve activity (MSNA) from the peroneal nerve in conscious humans to determine if unloading of cardiac baroreceptors during nonhypotensive lower body negative pressure (LBNP) increases sympathetic discharge to the leg muscles. LBNP from -5 to -15 mmHg had no effect on arterial pressure or heart rate but caused graded decreases in central venous pressure and corresponding large increases in peroneal MSNA. Total MSNA (burst frequency X mean burst amplitude) increased by 61 +/- 22% (P less than 0.05 vs. control) during LBNP at only -5 mmHg and rose progressively to a value that was 149 +/- 29% greater than control during LBNP at -15 mmHg (P less than 0.05). The major new conclusion is that nonhypotensive LBNP is a potent stimulus to muscle sympathetic outflow in the leg as well as the arm. During orthostatic stress in humans, the cardiac baroreflex appears to trigger a mass sympathetic discharge to the skeletal muscles in all of the extremities.


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 ◽  
...  

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.


2010 ◽  
Vol 109 (4) ◽  
pp. 996-1001 ◽  
Author(s):  
T. Hachiya ◽  
M. L. Walsh ◽  
M. Saito ◽  
A. P. Blaber

Central blood volume loss to venous pooling in the lower extremities and vasoconstrictor response are commonly viewed as key factors to distinguish between individuals with high and low tolerance to orthostatic stress. In this study, we analyzed calf vasoconstriction as a function of venous pooling during simulated orthostatic stress. We hypothesized that high orthostatic tolerance (OT) would be associated with greater vasoconstrictor responses to venous pooling compared with low OT. Nineteen participants underwent continuous stepped lower body negative pressure at −10, −20, −30, −40, −50, and −60 mmHg each for 5 min or until exhibiting signs of presyncope. Ten participants completed the lower body negative pressure procedure without presyncope and were categorized with high OT; the remaining nine were categorized as having low OT. Near-infrared spectroscopy measurements of vasoconstriction (Hachiya T, Blaber A, Saito M. Acta Physiologica 193: 117–127, 2008) in calf muscles, along with heart rate (HR) responses for each participant, were evaluated in relation to calf blood volume, estimated by plethysmography. The slopes of this relationship between vasoconstriction and blood volume were not different between the high- and low-tolerance groups. However, the onset of vasoconstriction in the high-tolerance group was delayed. Greater HR increments in the low-tolerance group were also observed as a function of lower limb blood pooling. The delayed vasoconstriction and slower HR increments in the high-tolerance group to similar venous pooling in the low group may suggest a greater vascular reserve and possible delayed reduction in venous return.


1994 ◽  
Vol 267 (2) ◽  
pp. H593-H604 ◽  
Author(s):  
D. K. Levenhagen ◽  
J. M. Evans ◽  
M. Wang ◽  
C. F. Knapp

The frequency response characteristics of human cardiovascular regulation during hypotensive stress have not been determined. We therefore exposed 10 male volunteers to seven frequencies (0.004–0.1 Hz) of oscillatory lower body negative pressure (OLBNP; 0–50 mmHg). Fourier spectra of arterial pressure (AP), central venous pressure (CVP), stroke volume (SV), cardiac output (CO), heart rate (HR), and total peripheral resistance (TPR) were determined and first harmonic mean, amplitude, and phase angles with respect to OLBNP are presented. AP was relatively well regulated as demonstrated by small oscillations in half amplitude (3.5 mmHg) that were independent of OLBNP frequency and similar to unstressed control spectra. Due to the biomechanics of the system, the magnitudes of oscillations in calf circumference (CC) and CVP decreased with increasing frequency; therefore, we normalized responses by these indexes of the fluid volume shifted. The ratios of oscillations in AP to oscillations in CC increased by an order of magnitude, whereas oscillations in CVP to oscillations in CC and oscillations in AP to oscillations in CVP both tripled between 0.004 and 0.1 Hz. Therefore, even though the amount of fluid shifted by OLBNP decreased with increasing frequency, the magnitude of both CVP and AP oscillations per volume of fluid shifted increased (peaking at 0.08 Hz). The phase relationships between variables, particularly the increasing lags in SV and TPR, but not CVP, indicated that efferent responses with lags of 5–6 s could account for the observed responses. We conclude that, at frequencies below 0.02 Hz, the neural system of humans functioned optimally in regulating AP; OLBNP-induced decreases in SV (by as much as 50%) were counteracted by appropriate oscillations in HR and TPR responses. As OLBNP frequency increased, SV, TPR, and HR oscillations increasingly lagged the input and became less optimally timed for AP regulation.


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