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

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. 125-132 ◽  
Author(s):  
Darrel P. FRANCIS ◽  
L. Ceri DAVIES ◽  
Keith WILLSON ◽  
Piotr PONIKOWSKI ◽  
Andrew J. S. COATS ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Heart Rate ◽  
Chronic Heart Failure ◽  
Spectral Power ◽  
Low Frequency ◽  
Periodic Breathing ◽  
Free Breathing ◽  
Very Low Frequency ◽  
Rr Interval

In chronic heart failure, very-low-frequency (VLF) oscillations (0.01–0.04 Hz) in heart rate and blood pressure may be related to periodic breathing, although the mechanism has not been fully characterized. Groups of ten patients with chronic heart failure and ten healthy controls performed voluntary periodic breathing with computer guidance, while ventilation, oxygen saturation, non-invasive blood pressure and RR interval were measured. In air, voluntary periodic breathing induced periodic desaturation and prominent VLF oscillations when compared with free breathing in both patients [RR interval spectral power from 179 to 358 ms2 (P < 0.05); systolic blood pressure (SBP) spectral power from 3.44 to 6.25 mmHg2 (P < 0.05)] and controls [RR spectral power from 1040 to 2307 ms2 (P < 0.05); SBP spectral power from 3.40 to 9.38 mmHg2 (P < 0.05)]. The peak in RR interval occurred 16–26 s before that in SBP, an anti-baroreflex pattern. When the patients followed an identical breathing pattern in hyperoxic conditions to prevent desaturation, the VLF RR interval spectral power was 50% lower (179.0±51.7 ms2; P < 0.01) and the VLF SBP spectral power was 44% lower (3.51±0.77 mmHg2; P < 0.01); similar effects were seen in controls (VLF RR power 20% lower, at 1847±899 ms2, P < 0.05; VLF SBP power 61% lower, at 3.68±0.92 mmHg2, P = 0.01). Low- and high-frequency spectral powers were not significantly affected. Thus periodic breathing causes oxygen-sensitive (and by implication chemoreflex-related) anti-baroreflex VLF oscillations in RR interval and blood pressure in both patients with chronic heart failure and normal controls.

Characterization of the role of endogenous nitric oxide in myogenic vascular oscillations during cooling-evoked hemodynamic perturbations of rats

2017 ◽  
Vol 95 (7) ◽  
pp. 803-810 ◽  
Author(s):  
Yi-Hsien Lin ◽  
Yia-Ping Liu ◽  
Yu-Chieh Lin ◽  
Po-Lei Lee ◽  
Che-Se Tung
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Heart Rate ◽  
Cold Stress ◽  
Low Frequency ◽  
Sympathetic Activation ◽  
Nitric Oxide Synthase Inhibitor ◽  
Dicrotic Notch ◽  
Endogenous Nitric Oxide

Rapid immersion of a rat’s limbs into 4 °C water, a model of cold stress, can elicit hemodynamic perturbations (CEHP). We previously reported that CEHP is highly relevant to sympathetic activation and nitric oxide production. This study identifies the role of nitric oxide in CEHP. Conscious rats were pretreated with the nitric oxide synthase inhibitor L-NAME (NG-nitro-l-arginine methyl ester) alone or following the removal of sympathetic influences using hexamethonium or guanethidine. Rats were then subjected to a 10 min cold-stress trial. Hemodynamic indices were telemetrically monitored throughout the experiment. The analyses included measurements of systolic blood pressure; heart rate; dicrotic notch; short-term cardiovascular oscillations and coherence between blood pressure variability and heart rate variability in regions of very low frequency (0.02–0.2 Hz), low frequency (0.2–0.6 Hz), and high frequency (0.6–3.0 Hz). We observed different profiles of hemodynamic reaction between hexamethonium and guanethidine superimposed on L-NAME, suggesting an essential role for a functional adrenal medulla release of epinephrine under cold stress. These results indicate that endogenous nitric oxide plays an important role in the inhibition of sympathetic activation and cardiovascular oscillations in CEHP.

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.

Role of cardiac output in mediating arterial blood pressure oscillations

1996 ◽  
Vol 271 (3) ◽  
pp. R641-R646 ◽  
Author(s):  
D. S. O'Leary ◽  
D. J. Woodbury
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Low Frequency ◽  
Left Ventricular ◽  
Right Atrial ◽  
Total Power ◽  
Av Block ◽  
Arterial Blood ◽  
Low Frequency Oscillations

The objective of this study was to determine the role of cardiac output in mediating spontaneous fluctuations in mean arterial pressure (MAP) conscious dogs. Dogs were chronically instrumented to monitor MAP and cardiac output. Atrioventricular (AV) block was induced, and left ventricular and right atrial electrodes were implanted. After recovery, MAP was observed for 5 min under two conditions: 1) normal variation in heart rate and cardiac output via triggering the ventricular stimulator with each atrial depolarization (effectively reversing the AV block, AV-linked stimulation) and 2) computer control of ventricular rate to maintain cardiac output constant on a by-beat basis at the same level as observed during normal variations in heart rate and cardiac output. When cardiac output was held constant, large-amplitude, low-frequency oscillations in MAP were readily apparent. Spectral analysis by fast Fourier transform revealed that during constant cardiac output the power observed at low frequencies in the MAP spectrum represented 95.0 +/- 2.7% of the total power compared with 75.5 +/- 4.6% during normal variations in heart rate and cardiac output (P < 0.05). In addition, when cardiac output was held constant, the power observed at higher frequencies markedly decreased from 24.5 +/- 4.6% of total power during AV-linked stimulation to only 5.0 +/- 2.7% of total power during constant cardiac output (P < 0.05). We conclude that low-frequency oscillations in MAP are due to changes in peripheral resistance, whereas a significant amount of high-frequency changes in MAP stems from spontaneous changes in cardiac output.

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

scholarly journals early diagnosis of the hemodynamic regulation disorders in orthostasis

2016 ◽  
Vol 1 (5) ◽  
pp. 30-34
Author(s):  
Мартынов ◽  
Ilya Martynov
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
High Frequency ◽  
Low Frequency ◽  
Orthostatic Test ◽  
Peripheral Vascular ◽  
High Frequency Oscillations ◽  
Low Frequency Oscillations ◽  
Vasomotor Regulation ◽  
Informative Content

The article deals with the informative content of spectral analysis of heart rate variability in the assessment of the regulatory impacts on the systemic hemodynamics during orthostatic test. It was observed that the patients who suffer from neurogenic syncope already at a young age had had a decrease in low frequency oscillations, as well as a decrease in peripheral vascular resistance during the test. It allows us to make a conclusion about the sympathetic vasomotor regulation dysfunction, even before the symptoms of orthostatic hypotension were evident. The decrease in the tonic vagal effect which follows from the depression of high-frequency oscillations, makes for increasing the chronotropic function of the heart and keeps a relative sympathetic predominance in order to maintain adequate level of blood pressure

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