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

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.

1988 ◽  
Vol 254 (4) ◽  
pp. H693-H701 ◽  
Author(s):  
K. G. Cornish ◽  
J. P. Gilmore ◽  
T. McCulloch

Conscious intact (I) and sinoaortic-denervated monkeys (SAD) were studied to determine the extent to which high-pressure receptors contribute to the maintenance of arterial blood pressure (BP) when venous return is decreased by hemorrhage (H) or lower body negative pressure (LBNP). In the I animals, mean BP did not decrease significantly until 5% of the estimated blood volume (EBV) was removed, whereas, with sinoaortic denervation, mean BP decreased significantly when less than 2% of EBV was removed. Left atrial pressure (LAP) decreased similarly in both groups of animals. In the I group during LBNP, mean BP did not change significantly, whereas pulse pressure decreased significantly when LBNP was decreased to -5 cmH2O. In the SAD animals, mean BP decreased significantly at an LBNP of -2 cmH2O, and at -5 cmH2O mean BP declined from 134.1 +/- 4 to 102.7 +/- 7 mmHg. LAP decreased similarly in both groups of animals. The data support the view that a nonhypotensive reduction in venous return unloads arterial baroreceptors sufficiently to activate the arterial baroreflex, probably through reductions in pulse pressure. In addition, low-pressure receptors by themselves do not appear to contribute importantly to blood pressure maintenance when venous return is decreased by either LBNP or a nonhypotensive hemorrhage.


1999 ◽  
Vol 277 (2) ◽  
pp. H576-H583 ◽  
Author(s):  
José González-Alonso ◽  
Ricardo Mora-Rodríguez ◽  
Edward F. Coyle

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.


Author(s):  
Arundhati Goley ◽  
A. Mooventhan ◽  
NK. Manjunath

Abstract Background Hydrotherapeutic applications to the head and spine have shown to improve cardiovascular and autonomic functions. There is lack of study reporting the effect of either neutral spinal bath (NSB) or neutral spinal spray (NSS). Hence, the present study was conducted to evaluate and compare the effects of both NSB and NSS in healthy volunteers. Methods Thirty healthy subjects were recruited and randomized into either neutral spinal bath group (NSBG) or neutral spinal spray group (NSSG). A single session of NSB, NSS was given for 15 min to the NSBG and NSSG, respectively. Assessments were taken before and after the interventions. Results Results of this study showed a significant reduction in low-frequency (LF) to high-frequency (HF) (LF/HF) ratio of heart rate variability (HRV) spectrum in NSBG compared with NSSG (p=0.026). Within-group analysis of both NSBG and NSSG showed a significant increase in the mean of the intervals between adjacent QRS complexes or the instantaneous heart rate (HR) (RRI) (p=0.002; p=0.009, respectively), along with a significant reduction in HR (p=0.002; p=0.004, respectively). But, a significant reduction in systolic blood pressure (SBP) (p=0.037) and pulse pressure (PP) (p=0.017) was observed in NSSG, while a significant reduction in diastolic blood pressure (DBP) (p=0.008), mean arterial blood pressure (MAP) (p=0.008) and LF/HF ratio (p=0.041) was observed in NSBG. Conclusion Results of the study suggest that 15 min of both NSB and NSS might be effective in reducing HR and improving HRV. However, NSS is particularly effective in reducing SBP and PP, while NSB is particularly effective in reducing DBP and MAP along with improving sympathovagal balance in healthy volunteers.


1996 ◽  
Vol 271 (2) ◽  
pp. H812-H822 ◽  
Author(s):  
W. C. Rose ◽  
J. S. Schwaber

Vagal control of the heart is the most rapidly responding limb of the arterial baroreflex. We created a mathematical model of the left heart and vascular system to evaluate the ability of heart rate to influence blood pressure. The results show that arterial pressure depends nonlinearly on rate and that changes in rate are of limited effectiveness, particularly when rate is increased above the basal level. A 10% change in heart rate from rest causes a change of only 2.4% in arterial pressure due to the reciprocal relation between heart rate and stroke volume; at higher rates, insufficient filling time causes stroke volume to fall. These findings agree well with published experimental data and challenge the idea that changes in heart rate alone can strongly and rapidly affect arterial pressure. Possible implications are that vagally mediated alterations in inotropic and dromotropic state, which are not included in this model, play important roles in the fast reflex control of blood pressure or that the vagal limb of the baroreflex is of rather limited effectiveness.


1992 ◽  
Vol 73 (5) ◽  
pp. 1946-1957 ◽  
Author(s):  
J. H. Muntinga ◽  
K. R. Visser

In 13 healthy volunteers a computerized experimental set-up was used to measure the electrical impedance of the upper arm at changing cuff pressure, together with the finger arterial blood pressure in the contralateral arm. On the basis of a model for the admittance response, the arterial blood volume per centimeter length (1.4 +/- 0.3 ml/cm), the venous blood volume as a percentage of the total blood compartment (49.2 +/- 12.6%), and the total arterial compliance as a function of mean arterial transmural pressure were estimated. The effective physiological arterial compliance amounted to 2.0 +/- 1.3 microliters.mmHg-1.cm-1 and the maximum compliance to 33.4 +/- 12.0 microliters.mmHg-1.cm-1. Additionally, the extravascular fluid volume expelled by the occluding cuff (0.3 +/- 0.3 ml/cm) was estimated. These quantities are closely related to patient-dependent sources of an unreliable blood pressure measurement and vary with changes in cardiovascular function, such as those found in hypertension. Traditionally, a combination of several methods is needed to estimate them. Such methods, however, usually neglect the contribution of extravascular factors.


1984 ◽  
Vol 62 (2) ◽  
pp. 137-147 ◽  
Author(s):  
John X. Wilson

The mammalian renin–angiotensin system appears to be involved in the maintenance of blood volume and pressure because (i) sodium depletion, hypovolemia, and hypotension increase renin levels, and (ii) administration of exogenous angiotensin II rapidly increases mineralocorticoid and antidiuretic hormone production, transepithelial ion transport, drinking behavior, and peripheral vascular resistance. Are these also the physiological properties of the renin–angiotensin system in nonmammalian species? Signals for altered levels of renin activity have yet to be conclusively identified in nonmammalian vertebrates, but circulating renin levels are elevated by hypotension in teleost fish and birds. Systemic injection of angiotensin II causes an increase in arterial blood pressure in all the vertebrates studied, suggesting that barostatic control is a universal function of this hormone. Angiotensin II alters vascular tone by direct action on arteriolar muscles in some species, but at concentrations of the hormone which probably are unphysiological. More generally, angiotensin II increases blood pressure indirectly, by acting on the sympathetic nervous system. Catecholamines, derived from chromaffin cells and (or) from peripheral adrenergic nerves, mediate some portion of the vasopressor response to angiotensin II in cyclostomes, elasmobranchs, teleosts, amphibians, reptiles, mammals, and birds. Alteration of sympathetic outflow is a prevalent mechanism through which the renin–angiotensin system may integrate blood volume, cardiac output, and peripheral vascular resistance to achieve control of blood pressure and adequate perfusion of tissues.


2011 ◽  
Vol 110 (4) ◽  
pp. 917-925 ◽  
Author(s):  
Gregory S. H. Chan ◽  
Philip N. Ainslie ◽  
Chris K. Willie ◽  
Chloe E. Taylor ◽  
Greg Atkinson ◽  
...  

The Windkessel properties of the vasculature are known to play a significant role in buffering arterial pulsations, but their potential importance in dampening low-frequency fluctuations in cerebral blood flow has not been clearly examined. In this study, we quantitatively assessed the contribution of arterial Windkessel (peripheral compliance and resistance) in the dynamic cerebral blood flow response to relatively large and acute changes in blood pressure. Middle cerebral artery flow velocity (MCAV; transcranial Doppler) and arterial blood pressure were recorded from 14 healthy subjects. Low-pass-filtered pressure-flow responses (<0.15 Hz) during transient hypertension (intravenous phenylephrine) and hypotension (intravenous sodium nitroprusside) were fitted to a two-element Windkessel model. The Windkessel model was found to provide a superior goodness of fit to the MCAV responses during both hypertension and hypotension ( R2 = 0.89 ± 0.03 and 0.85 ± 0.05, respectively), with a significant improvement in adjusted coefficients of determination ( P < 0.005) compared with the single-resistance model ( R2 = 0.62 ± 0.06 and 0.61 ± 0.08, respectively). No differences were found between the two interventions in the Windkessel capacitive and resistive gains, suggesting similar vascular properties during pressure rise and fall episodes. The results highlight that low-frequency cerebral hemodynamic responses to transient hypertension and hypotension may include a significant contribution from the mechanical properties of vasculature and, thus, cannot solely be attributed to the active control of vascular tone by cerebral autoregulation. The arterial Windkessel should be regarded as an important element of dynamic cerebral blood flow modulation during large and acute blood pressure perturbation.


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