Relationship between low-frequency fluctuations in arterial blood pressure and tissue blood volume

1999 ◽  
Author(s):  
Meir Nitzan ◽  
Anatoly Babchenko ◽  
Boris Khanokh
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Blood Volume ◽  
Low Frequency ◽  
Arterial Blood ◽  
Frequency Fluctuations

Resonance in a mathematical model of baroreflex control: arterial blood pressure waves accompanying postural stress

2005 ◽  
Vol 288 (6) ◽  
pp. R1637-R1648 ◽  
Author(s):  
Peter E. Hammer ◽  
J. Philip Saul
Keyword(s):  
Blood Pressure ◽  
Mathematical Model ◽  
Blood Volume ◽  
Low Frequency ◽  
Pressure Waves ◽  
Central Blood Volume ◽  
Arterial Baroreflex ◽  
Arterial Blood ◽  
Gain Margin ◽  
The Stability

A mathematical model of the arterial baroreflex was developed and used to assess the stability of the reflex and its potential role in producing the low-frequency arterial blood pressure oscillations called Mayer waves that are commonly seen in humans and animals in response to decreased central blood volume. The model consists of an arrangement of discrete-time filters derived from published physiological studies, which is reduced to a numerical expression for the baroreflex open-loop frequency response. Model stability was assessed for two states: normal and decreased central blood volume. The state of decreased central blood volume was simulated by decreasing baroreflex parasympathetic heart rate gain and by increasing baroreflex sympathetic vaso/venomotor gains as occurs with the unloading of cardiopulmonary baroreceptors. For the normal state, the feedback system was stable by the Nyquist criterion (gain margin = 0.6), but in the hypovolemic state, the gain margin was small (0.07), and the closed-loop frequency response exhibited a sharp peak (gain of 11) at 0.07 Hz, the same frequency as that observed for arterial pressure fluctuations in a group of healthy standing subjects. These findings support the theory that stresses affecting central blood volume, including upright posture, can reduce the stability of the normally stable arterial baroreflex feedback, leading to resonance and low-frequency blood pressure waves.

Supine exercise restores arterial blood pressure and skin blood flow despite dehydration and hyperthermia

1999 ◽  
Vol 277 (2) ◽  
pp. H576-H583 ◽  
Author(s):  
José González-Alonso ◽  
Ricardo Mora-Rodríguez ◽  
Edward F. Coyle
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Blood Volume ◽  
Plasma Catecholamines ◽  
Central Blood Volume ◽  
Vascular Conductance ◽  
Arterial Blood ◽  
Cutaneous Vascular Conductance

We determined whether the deleterious effects of dehydration and hyperthermia on cardiovascular function during upright exercise were attenuated by elevating central blood volume with supine exercise. Seven trained men [maximal oxygen consumption (V˙o 2 max) 4.7 ± 0.4 l/min (mean ± SE)] cycled for 30 min in the heat (35°C) in the upright and in the supine positions (V˙o 2 2.93 ± 0.27 l/min) while maintaining euhydration by fluid ingestion or while being dehydrated by 5% of body weight after 2 h of upright exercise. When subjects were euhydrated, esophageal temperature (Tes) was 37.8–38.0°C in both body postures. Dehydration caused equal hyperthermia during both upright and supine exercise (Tes = 38.7–38.8°C). During upright exercise, dehydration lowered stroke volume (SV), cardiac output, mean arterial pressure (MAP), and cutaneous vascular conductance and increased heart rate and plasma catecholamines [30 ± 6 ml, 3.0 ± 0.7 l/min, 6 ± 2 mmHg, 22 ± 8%, 14 ± 2 beats/min, and 50–96%, respectively; all P < 0.05]. In contrast, during supine exercise, dehydration did not cause significant alterations in MAP, cutaneous vascular conductance, or plasma catecholamines. Furthermore, supine versus upright exercise attenuated the increases in heart rate (7 ± 2 vs. 9 ± 1%) and the reductions in SV (13 ± 4 vs. 21 ± 3%) and cardiac output (8 ± 3 vs. 14 ± 3%) (all P< 0.05). These results suggest that the decline in cutaneous vascular conductance and the increase in plasma norepinephrine concentration, independent of hyperthermia, are associated with a reduction in central blood volume and a lower arterial blood pressure.

A sudden arterial blood pressure decrease is compensated by an increase in intracranial blood volume

2002 ◽  
Vol 249 (5) ◽  
pp. 538-541 ◽  
Author(s):  
Bernhard Rosengarten ◽  
Damian Rüskes ◽  
Irene Mendes ◽  
Erwin Stolz
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Blood Volume ◽  
Blood Pressure Decrease ◽  
Arterial Blood ◽  
Pressure Decrease

scholarly journals Effects of glucagon-like peptide-1(7-36) amide on neurohypophysial and cardiovascular functions under hypo- or normotensive hypovolaemia in the rat

2002 ◽  
Vol 172 (2) ◽  
pp. 303-310 ◽  
Author(s):  
E Bojanowska ◽  
B Stempniak
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Blood Volume ◽  
Mean Arterial Blood Pressure ◽  
Volume Depletion ◽  
Arterial Blood ◽  
The Mean ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Cardiovascular Functions

To date, glucagon-like peptide 1(7-36) amide (tGLP-1) has been found to affect the neurohypophysial and cardiovascular functions in normotensive and normovolaemic rats. The aim of the present study was to investigate possible effects of tGLP-1 on the mean arterial blood pressure and the release of vasopressin and oxytocin under conditions of blood volume depletion in the rat. In the first series of experiments, the animals were injected i.p. with either 0.15 M saline or 30% polyethylene glycol (PEG). PEG caused an 18% reduction of blood volume 1 h after injection. No significant changes in the mean arterial blood pressure were found in either normo- or hypovolaemic rats during the experiment. tGLP-1 injected i.c.v. at a dose of 1 microg/5 microl 1 h after the i.p. injection increased similarly the arterial blood pressure in normo- and hypovolaemic rats. The plasma vasopressin/oxytocin concentrations were markedly elevated in hypovolaemic animals and tGLP-1 further augmented the release of both hormones. In the second study, hypovolaemia was induced by double blood withdrawal. The haemorrhage resulted in a marked decrease of the mean arterial blood pressure and in the elevated plasma vasopressin/oxytocin concentrations. tGLP-1 injected immediately after the second blood withdrawal increased the arterial blood pressure. In parallel, tGLP-1 enhanced significantly vasopressin and oxytocin secretion when compared with haemorrhaged, saline-injected rats. The results of this study indicate that tGLP-1 may affect the arterial blood pressure and the secretion of neurohypophysial hormones under pathological conditions brought about by blood volume depletion.

Does nitric oxide buffer arterial blood pressure variability in humans?

2002 ◽  
Vol 93 (4) ◽  
pp. 1466-1470 ◽  
Author(s):  
William H. Cooke ◽  
Rong Zhang ◽  
Julie H. Zuckerman ◽  
Jian Cui ◽  
Thad E. Wilson ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Animal Studies ◽  
Transfer Functions ◽  
Body Position ◽  
Low Frequency ◽  
Power Spectral Analysis ◽  
Arterial Blood

Animal studies suggest that nitric oxide (NO) plays an important role in buffering short-term arterial pressure variability, but data from humans addressing this hypothesis are scarce. We evaluated the effects of NO synthase (NOS) inhibition on arterial blood pressure (BP) variability in eight healthy subjects in the supine position and during 60° head-up tilt (HUT). Systemic NOS was blocked by intravenous infusion of N G-monomethyl-l-arginine (l-NMMA). Electrocardiogram and beat-by-beat BP in the finger (Finapres) were recorded continuously for 6 min, and brachial cuff BP was recorded before and after l-NMMA in each body position. BP and R-R variability and their transfer functions were quantified by power spectral analysis in the low-frequency (LF; 0.05–0.15 Hz) and high-frequency (HF; 0.15–0.35 Hz) ranges.l-NMMA infusion increased supine BP (systolic, 109 ± 4 vs. 122 ± 3 mmHg, P = 0.03; diastolic, 68 ± 2 vs. 78 ± 3 mmHg, P = 0.002), but it did not affect supine R-R interval or BP variability. Beforel-NMMA, HUT decreased HF R-R variability ( P= 0.03), decreased transfer function gain (LF, 12 ± 2 vs. 5 ± 1 ms/mmHg, P = 0.007; HF, 18 ± 3 vs. 3 ± 1 ms/mmHg, P = 0.002), and increased LF BP variability ( P < 0.0001). After l-NMMA, HUT resulted in similar changes in BP and R-R variability compared with tilt without l-NMMA. Increased supine BP afterl-NMMA with no effect on BP variability during HUT suggests that tonic release of NO is important for systemic vascular tone and thus steady-state arterial pressure, but NO does not buffer dynamic BP oscillations in humans.

Empirical and theoretical analysis of the extremely low frequency arterial blood pressure power spectrum in unanesthetized rat

2006 ◽  
Vol 291 (6) ◽  
pp. H2816-H2824 ◽  
Author(s):  
David R. Brown ◽  
Lisa A. Cassis ◽  
Dennis L. Silcox ◽  
Laura V. Brown ◽  
David C. Randall
Keyword(s):  
Blood Pressure ◽  
Time Series ◽  
Power Spectrum ◽  
Arterial Blood Pressure ◽  
Low Frequency ◽  
Absolute Difference ◽  
Frequency Range ◽  
Low Frequencies ◽  
Extremely Low Frequency ◽  
Arterial Blood

The slope of the log of power versus the log of frequency in the arterial blood pressure (BP) power spectrum is classically considered constant over the low-frequency range (i.e., “fractal” behavior), and is quantified by β in the relationship “1/ fβ.” In practice, the fractal range cannot extend to indefinitely low frequencies, but factor(s) that terminate this behavior, and determine β, are unclear. We present 1) data in rats ( n = 8) that reveal an extremely low frequency spectral region (0.083–1 cycle/h), where β approaches 0 (i.e., the “shoulder”); and 2) a model that 1) predicts realistic values of β within that range of the spectrum that conforms to fractal dynamics (∼1–60 cycles/h), 2) offers an explanation for the shoulder, and 3) predicts that the “successive difference” in mean BP (mBP) is an important parameter of circulatory function. We recorded BP for up to 16 days. The absolute difference between successive mBP samples at 0.1 Hz (the successive difference, or Δ) was 1.87 ± 0.21 mmHg (means ± SD). We calculated β for three frequency ranges: 1) 0.083–1; 2) 1–6; and 3) 6–60 cycles/h. The β for all three regions differed ( P < 0.01). For the two higher frequency ranges, β indicated a fractal relationship (β6–60/h = 1.27 ± 0.01; β1–6/h = 1.80 ± 0.16). Conversely, the slope of the lowest frequency region (i.e., the shoulder) was nearly flat (β0.083–1 /h = 0.32 ± 0.28). We simulated the BP time series as a random walk about 100 mmHg with ranges above and below of 10, 30, and 50 mmHg and with Δ from 0.5 to 2.5. The spectrum for the conditions mimicking actual BP time series (i.e., range, 85–115 mmHg; Δ, 2.00) resembled the observed spectra, with β in the lowest frequency range = 0.207 and fractal-like behavior in the two higher frequency ranges (β = 1.707 and 2.057). We suggest that the combined actions of mechanisms limiting the excursion of arterial BP produce the shoulder in the spectrum and that Δ contributes to determining β.

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