Hysteresis in response to descending and ascending lower-body negative pressure

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.

1994 ◽  
Vol 267 (1) ◽  
pp. R26-R33 ◽  
Author(s):  
G. C. Butler ◽  
Y. Yamamoto ◽  
R. L. Hughson

We have shown previously that the heart rate variability (HRV) signal is fractal in nature with a high degree of complexity, as given by the calculated fractal dimension (DF). We have also reported that loss of complexity, as indicated by a reduction in DF of HRV, is associated with orthostatic hypotension and impending syncope. To extend this investigation of cardiovascular responses, we have investigated the signal characteristics of short-term systolic blood pressure variability (BPV) coincident with measurements of HRV during orthostatic stress. Eight healthy men completed a test protocol of 20 min supine rest followed sequentially by 10 min at each of -5, -15, -25, -40, and -50 mmHg lower body negative pressure (LBNP) and 10 min supine recovery. We found that resting BPV and HRV were fractal with approximately 70% of both variables in the fractal component of the variability signal. The slope of the 1/f beta relationship was 1.16 +/- 0.12 for HRV and 2.31 +/- 0.17 for BPV. With increasing levels of orthostatic stress, the 1/f beta slope of HRV increased significantly to 1.68 +/- 0.08 at -50 mmHg LBNP, whereas the 1/f beta slope was unchanged for BPV. Indicators of parasympathetic and sympathetic nervous system activity derived from heart rate variability suggested reduced and increased values, respectively, as the LBNP increased. These data indicate important differences in heart rate and blood pressure control under 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.


1997 ◽  
Vol 29 (Supplement) ◽  
pp. 36
Author(s):  
S. M.C. Lee ◽  
L. Steinmann ◽  
M. Wood ◽  
L. Dussack ◽  
S. M. Fortney

1990 ◽  
Vol 68 (1) ◽  
pp. 355-362 ◽  
Author(s):  
J. M. Overton ◽  
C. M. Tipton

To determine whether hindlimb suspension is associated with the development of cardiovascular deconditioning, male rats were studied before and after undergoing one of three treatment conditions for 9 days: 1) cage control (n = 15, CON), 2) horizontal suspension (n = 15, HOZ), and 3) head-down suspension (n = 18, HDS). Testing included lower body negative pressure administered during chloralose-urethan anesthesia and graded doses of sympathomimetic agents (norepinephrine, phenylephrine, and tyramine) administered to conscious unrestrained animals. Both HDS and HOZ were associated with a small decrease in the hypotensive response to lower body negative pressure. The HOZ group, but not the HDS group, exhibited augmented reflex tachycardia. Furthermore, both HDS and HOZ groups manifested reduced pressor responses to phenylephrine after treatment. These reductions were associated with significantly attenuated increases in mesenteric vascular resistance. However, baroreflex control of heart rate was not altered by the treatment conditions. Collectively, these results indicate that 9 days of HDS in rats does not elicit hemodynamic response patterns generally associated with cardiovascular deconditioning induced by hypogravic conditions.


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.


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