Very low frequency blood pressure fluctuations: not only myogenic responsiveness

2008 ◽  
Vol 26 (6) ◽  
pp. 1065-1068 ◽  
Author(s):  
Claude Julien ◽  
J Philip Saul ◽  
Gianfranco Parati
Keyword(s):  
Blood Pressure ◽  
Pressure Fluctuations ◽  
Low Frequency ◽  
Very Low Frequency

Impaired sympathetic response before intradialytic hypotension: a study based on spectral analysis of heart rate and pressure variability

1999 ◽  
Vol 96 (1) ◽  
pp. 23-31 ◽  
Author(s):  
Gualtiero PELOSI ◽  
Michele EMDIN ◽  
Clara CARPEGGIANI ◽  
Maria Aurora MORALES ◽  
Marcello PIACENTI ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Pressure Fluctuations ◽  
Power Spectra ◽  
Low Frequency ◽  
Autonomic Response ◽  
Dialysis Session ◽  
Intradialytic Hypotension ◽  
Sympathetic Response ◽  
A Minor

The purpose of this study was to evaluate the autonomic response to standard haemodialysis and the changes associated with the onset of intradialytic hypotension in 12 normotensive patients with uraemia. Power spectra of R–R interval and of blood pressure fluctuations were obtained during a standard dialysis session and estimated in the low-frequency (LF, 30–150 ;mHz) and high-frequency (HF, 150–400 ;mHz) range. The absolute power of the LF component of blood pressure variations and the LF/HF ratio of R–R interval were assumed as indexes of sympathetic activity. Standard haemodialysis induced hypotension in six patients (unstable) while a minor pressure decline was present in the other six (stable). Normalized blood volume before dialysis and percentage volume reduction were similar in the two groups. Tachycardia in response to pressure and volume decrease was more pronounced in stable than in unstable patients, as evidenced by a higher slope of the relation between R–R interval and systolic blood pressure (7.9 versus 0.9 ;ms/mmHg, P< 0.01). Sympathetic tone was enhanced during early dialysis in all patients (+2±1 for R–R LF/HF ratio, +2.4±0.6 ;mmHg2 and +7.2±2 ;mmHg2 for absolute LF power of diastolic and of systolic blood pressure respectively, P< 0.05), compared with baseline predialysis values. During late dialysis, unstable patients showed an impairment of sympathetic activation which preceded hypotension and was maximal during the crisis (-2.9±1.4 for R–R LF/HF ratio, -2.7±1.4 ;mmHg2 and -8.6±4.0 ;mmHg2 for absolute LF power of diastolic and of systolic blood pressure respectively, P< 0.05). On the contrary, stable patients showed constantly elevated indexes (+3.7±1.4 for R–R LF/HF ratio, +5.9±2.7 ;mmHg2 and +13.3±6.2 ;mmHg2 for LF of diastolic and of systolic blood pressure, P< 0.05). Values returned to predialysis levels after the end of the dialysis session in all patients. We conclude that standard haemodialysis activates a marked and reversible sympathetic response in both stable and unstable uraemic patients. However, in unstable patients, such activation is impaired in late dialysis, therefore contributing to the onset of the hypotensive crisis.

scholarly journals Dynamic cerebral autoregulation during passive heat stress in humans

2009 ◽  
Vol 296 (5) ◽  
pp. R1598-R1605 ◽  
Author(s):  
David A. Low ◽  
Jonathan E. Wingo ◽  
David M. Keller ◽  
Scott L. Davis ◽  
Jian Cui ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heat Stress ◽  
Transfer Function ◽  
High Frequency ◽  
Cerebral Autoregulation ◽  
Low Frequency ◽  
Passive Heating ◽  
Frequency Range ◽  
Very Low Frequency ◽  
Dynamic Cerebral Autoregulation

This study tested the hypothesis that passive heating impairs cerebral autoregulation. Transfer function analyses of resting arterial blood pressure and middle cerebral artery blood velocity (MCA Vmean), as well as MCA Vmean and blood pressure responses to rapid deflation of previously inflated thigh cuffs, were examined in nine healthy subjects under normothermic and passive heat stress (increase core temperature 1.1 ± 0.2°C, P < 0.001) conditions. Passive heating reduced MCA Vmean [change (Δ) of 8 ± 8 cm/s, P = 0.01], while blood pressure was maintained (Δ −1 ± 4 mmHg, P = 0.36). Coherence was decreased in the very-low-frequency range during heat stress (0.57 ± 0.13 to 0.26 ± 0.10, P = 0.001), but was >0.5 and similar between normothermia and heat stress in the low- (0.07–0.20 Hz, P = 0.40) and high-frequency (0.20–0.35 Hz, P = 0.12) ranges. Transfer gain was reduced during heat stress in the very-low-frequency (0.88 ± 0.38 to 0.59 ± 0.19 cm·s−1·mmHg−1, P = 0.02) range, but was unaffected in the low- and high-frequency ranges. The magnitude of the decrease in blood pressure (normothermia: 20 ± 4 mmHg, heat stress: 19 ± 6 mmHg, P = 0.88) and MCA Vmean (13 ± 4 to 12 ± 6 cm/s, P = 0.59) in response to cuff deflation was not affected by the thermal condition. Similarly, the rate of regulation of cerebrovascular conductance (CBVC) after cuff release (0.44 ± 0.22 to 0.38 ± 0.13 ΔCBVC units/s, P = 0.16) and the time for MCA Vmean to recover to precuff deflation baseline (10.0 ± 7.9 to 8.7 ± 4.9 s, P = 0.77) were not affected by heat stress. Counter to the proposed hypothesis, similar rate of regulation responses suggests that heat stress does not impair the ability to control cerebral perfusion after a rapid reduction in perfusion pressure, while reduced transfer function gain and coherence in the very-low-frequency range during heat stress suggest that dynamic cerebral autoregulation is improved during spontaneous oscillations in blood pressure within this frequency range.

Very-low-frequency oscillations in heart rate and blood pressure in periodic breathing: role of the cardiovascular limb of the hypoxic chemoreflex

2000 ◽  
Vol 99 (2) ◽  
pp. 125 ◽  
Author(s):  
Darrel P. FRANCIS ◽  
L. Ceri DAVIES ◽  
Keith WILLSON ◽  
Piotr PONIKOWSKI ◽  
Andrew J.S. COATS ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Low Frequency ◽  
Periodic Breathing ◽  
Very Low Frequency ◽  
Low Frequency Oscillations

scholarly journals Cooling-Evoked Hemodynamic Perturbations Facilitate Sympathetic Activity with Subsequent Myogenic Vascular Oscillations via Alpha2-Adrenergic Receptors

2017 ◽  
pp. 449-457 ◽  
Author(s):  
Y.-H. LIN ◽  
Y.-P. LIU ◽  
Y.-C. LIN ◽  
P.-L. LEE ◽  
C.-S. TUNG
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Pressor Response ◽  
Low Frequency ◽  
Power Spectral Analysis ◽  
Sprague Dawley ◽  
Cold Stimulation ◽  
Very Low Frequency ◽  
Power Spectral ◽  
Sprague Dawley Rats

This study extends our previous work by examining the effects of alpha2-adrenoceptors under cold stimulation involving the increase of myogenic vascular oscillations as increases of very-low-frequency and low-frequency of the blood pressure variability. Forty-eight adult male Sprague-Dawley rats were randomly divided into four groups: vehicle; yohimbine; hexamethonium+yohimbine; guanethidine+yohimbine. Systolic blood pressure, heart rate, power spectral analysis of spontaneous blood pressure and heart rate variability and spectral coherence at very-low-frequency (0.02 to 0.2 Hz), low-frequency (0.2 to 0.6 Hz), and high-frequency (0.6 to 3.0 Hz) regions were monitored using telemetry. Key findings are as follows: 1) Cooling-induced pressor response was attenuated by yohimbine and further attenuated by hexamethonium+yohimbine and guanethidine+yohimbine, 2) Cooling-induced tachycardia response of yohimbine was attenuated by hexame-thonium+yohimbine and guanethidine+yohimbine, 3) Different patterns of power spectrum reaction and coherence value compared hexamethonium+yohimbine and guanethi-dine+yohimbine to yohimbine alone under cold stimulation. The results suggest that sympathetic activation of the postsynaptic alpha2-adrenoceptors causes vasoconstriction and heightening myogenic vascular oscillations, in turn, may increase blood flow to prevent tissue damage under stressful cooling challenge.

A common origin of the very low frequency heart rate and blood pressure variability—a new insight into an old debate

2002 ◽  
Vol 96 (2) ◽  
pp. 140-148 ◽  
Author(s):  
Ron J Leor-Librach ◽  
Ben-Zion Bobrovsky ◽  
Sarah Eliash ◽  
Elieser Kaplinsky
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Pressure Variability ◽  
Low Frequency ◽  
Common Origin ◽  
Very Low Frequency ◽  
Insight Into

Hemodynamic regulation: investigation by spectral analysis

1985 ◽  
Vol 249 (4) ◽  
pp. H867-H875 ◽  
Author(s):  
S. Akselrod ◽  
D. Gordon ◽  
J. B. Madwed ◽  
N. C. Snidman ◽  
D. C. Shannon ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Spectral Analysis ◽  
Pressure Fluctuations ◽  
Low Frequency ◽  
Cardiovascular Control ◽  
Respiratory Frequency ◽  
Atrial Pacing ◽  
Loop Model ◽  
Short Term ◽  
Renin Angiotensin

We investigated the hypothesis that beat-to-beat variability in hemodynamic parameters reflects the dynamic interplay between ongoing perturbations to circulatory function and the compensatory response of short-term cardiovascular control systems. Spontaneous fluctuations in heart rate (HR), arterial blood pressure, and respiration were analyzed by spectral analysis in the 0.02- to 1-Hz frequency range. A simple closed-loop model of short-term cardiovascular control was proposed and evaluated in a series of experiments: pharmacological blockades of the parasympathetic, alpha-sympathetic, beta-sympathetic, and renin-angiotensin systems were used to open the principal control loops in order to examine changes in the spectral pattern of the fluctuations. Atrial pacing was used to examine blood pressure variability in the absence of HR variability. We found that respiratory frequency fluctuations in HR are parasympathetically mediated and that blood pressure fluctuations at this frequency result almost entirely from the direct effect of centrally mediated HR fluctuations. The sympathetic nervous system appears to be too sluggish to mediate respiratory frequency variations. Low-frequency (0.02-0.09 Hz) fluctuations in HR are jointly mediated by the parasympathetic and beta-sympathetic systems and appear to compensate for blood pressure fluctuations at this frequency. Low-frequency blood pressure fluctuations are probably due to variability in vasomotor activity which is normally damped by renin-angiotensin system activity. Blockade of the alpha-adrenergic system, however, does not significantly alter low-frequency blood pressure fluctuations.

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