Heart rate response to hemorrhage-induced 0.05-Hz oscillations in arterial pressure in conscious dogs

1991 ◽  
Vol 260 (4) ◽  
pp. H1248-H1253 ◽  
Author(s):  
J. B. Madwed ◽  
R. J. Cohen
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Low Frequency ◽  
Respiratory Frequency ◽  
Conscious Dogs ◽  
Reflex Response ◽  
Reflex Mechanism ◽  
Effector Mechanism ◽  
Low Frequency Oscillations ◽  
Cross Correlation Analysis

We have previously reported that oscillations at 0.05 Hz can be generated by a simple computer model incorporating a negative-feedback reflex mechanism and an effector mechanism with a time delay. Computer simulations by inhibiting the vagal effector mechanism and activating the adrenergic effector mechanism elicited low-frequency oscillations at a frequency of 0.05 Hz in heart rate. We have observed that the cardiovascular system of the conscious dog, when stressed by the loss of blood, generates oscillations in arterial pressure and heart rate at a frequency of 0.05 Hz. We investigated in six conscious dogs the role of the sympathetic and parasympathetic nervous systems in generating these heart rate oscillations. During baseline conditions, the predominant peak in the arterial pressure and heart rate power spectra was located at the respiratory frequency, while the low-frequency oscillations were small. After a 30-ml/kg hemorrhage or after an 8-, 15-, or 30-ml/kg hemorrhage with glycopyrrolate, a muscarinic-blocking agent, low-frequency oscillations at a frequency of 0.05 Hz predominated, while the respiratory frequency oscillations were negligible. Since respiratory frequency oscillations have been reported to reflect vagal activity, and since the low-frequency oscillations were present after vagal blockade, these hemorrhage-induced low-frequency oscillations in heart rate may be primarily mediated by the cardiac sympathetic nerves. Also cross-correlation analysis between arterial pressure and heart rate showed that a change in arterial pressure caused an opposite change in heart rate with a delay of 2-5 s. We conclude that hemorrhage-induced oscillations in heart rate at 0.05 Hz represent the arterial baroreceptor-beta-sympathetic reflex response to underlying arterial pressure oscillations.

Prostacyclin reduces "preload" in conscious dogs via a vagal reflex mechanism

1987 ◽  
Vol 253 (6) ◽  
pp. H1477-H1483
Author(s):  
D. M. Nganele ◽  
T. H. Hintze
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Left Ventricular ◽  
Vagal Afferents ◽  
Conscious Dogs ◽  
Reflex Mechanism ◽  
Capacitance Vessels ◽  
Preload Reduction ◽  
Cardiopulmonary Receptors ◽  
Electrical Pacing

The purpose of this study was to determine the effects of prostacyclin on left ventricular (LV) preload in conscious dogs. LV end-diastolic diameter (LV EDD) was used as an index of preload. Because prostacyclin reduces arterial pressure, data were sampled when mean arterial pressure, heart rate, and first derivative of LV pressure (dP/dt) had returned to control levels. There was no dose-response relationship in the preload reduction to prostacyclin, the threshold dose being 0.1 microgram/kg. Intravenous prostacyclin (2.0 micrograms/kg) reduced LV EDD 2.9 +/- 0.5% from 36 +/- 2.2 mm, (P less than 0.01). With heart rate held constant (146 +/- 2.5 beats/min) by electrical pacing, prostacyclin still reduced LV EDD by 4.0 +/- 1.0% from 32 +/- 2.5 mm (P less than 0.05). Intravenous administration of arachidonic acid (500 micrograms/kg) gave similar results. The magnitude of the preload response to prostacyclin was similar to that of nitroglycerin (25 micrograms/kg). Prazosin (1 mg/kg) or bilateral cervical vagal section completely abolished the preload response to prostacyclin but not to nitroglycerin. We, therefore, propose a mechanism where prostacyclin activates cardiopulmonary receptors with vagal afferents that results in a withdrawal of peripheral sympathetic tone to capacitance vessels to reduce preload, in contrast to nitroglycerin, whose mechanism of action is most probably a direct effect on capacitance vessels.

Low-frequency oscillations in arterial pressure and heart rate: a simple computer model

1989 ◽  
Vol 256 (6) ◽  
pp. H1573-H1579 ◽  
Author(s):  
J. B. Madwed ◽  
P. Albrecht ◽  
R. G. Mark ◽  
R. J. Cohen
Keyword(s):  
Heart Rate ◽  
Nervous System ◽  
Computer Model ◽  
Low Frequency ◽  
Beta Adrenergic ◽  
Simple Computer ◽  
Effector Mechanism ◽  
Arterial Blood ◽  
Low Frequency Oscillations ◽  
Effector Mechanisms

We have previously reported that low-frequency oscillations in arterial blood pressure (ABP) and heart rate (HR) occur when conscious dogs experience severe blood loss. These low-frequency oscillations are generated by enhancement of the sympathetic nervous system and inhibition of the parasympathetic nervous system. We have developed a simple computer model to elucidate those properties critical to the generation of these oscillations. Our model incorporates several important features: 1) arterial baroreceptor feedback loops, which relate ABP to targeted HR and total peripheral resistance (TPR) values; 2) two effector outputs, HR and TPR, which are controlled by the outputs of vagal, beta-adrenergic, and alpha-adrenergic effector mechanisms; 3) a fixed beat-to-beat stroke volume; and 4) a wind-kessel model, which represents the peripheral circulation. Each effector mechanism is modeled as a low-pass filter in series with a delay. The vagal effector mechanism slows the HR after a 100-ms delay and reaches maximal HR at that time. The beta-adrenergic effector mechanism speeds HR after a 2.5-s delay and then increases to maximal HR 7.5 s later. The alpha-adrenergic effector mechanism begins vasoconstriction after a 5-s delay and then reaches maximal contraction 15 s later. Computer simulations of inhibition of the vagal effector mechanism and activation of the adrenergic effector mechanisms elicit low-frequency oscillations in ABP and HR. These oscillations are similar to those observed experimentally in the dog during hemorrhage. We conclude that the slow temporal response of the alpha-adrenergic effector mechanism controlling TPR is the critical element in predicting the observed low-frequency oscillations in ABP and HR.

Impact of acute hypoxia on heart rate and blood pressure variability in conscious dogs

2000 ◽  
Vol 279 (5) ◽  
pp. H2344-H2349 ◽  
Author(s):  
Fumihiko Yasuma ◽  
Jun-Ichiro Hayano
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Minute Ventilation ◽  
Low Frequency ◽  
Frequency Component ◽  
Conscious Dogs ◽  
High Frequency Component ◽  
Progressive Hypoxia ◽  
Cardiovascular Variables

To examine whether the impacts of hypoxia on autonomic regulations involve the phasic modulations as well as tonic controls of cardiovascular variables, heart rate, blood pressure, and their variability during isocapnic progressive hypoxia were analyzed in trained conscious dogs prepared with a permanent tracheostomy and an implanted blood pressure telemetry unit. Data were obtained at baseline and when minute ventilation (V˙i) first reached 10 (V˙i10), 15 (V˙i15), and 20 (V˙i20) l/min during hypoxia. Time-dependent changes in the amplitudes of the high-frequency component of the R-R interval (RRIHF) and the low-frequency component of mean arterial pressure (MAPLF) were analyzed by complex demodulation. In a total of 47 progressive hypoxic runs in three dogs, RRIHF decreased atV˙i15 and V˙i20 and MAPLF increased at V˙i10 and V˙i15 but not atV˙i20, whereas heart rate and arterial pressure increased progressively with advancing hypoxia. We conclude that the autonomic responses to isocapnic progressive hypoxia involve tonic controls and phasic modulations of cardiovascular variables; the latter may be characterized by a progressive reduction in respiratory vagal modulation of heart rate and a transient augmentation in low-frequency sympathetic modulation of blood pressure.

Vascular resistance and arterial pressure low-frequency oscillations in the anesthetized dog

1995 ◽  
Vol 268 (1) ◽  
pp. H7-H16 ◽  
Author(s):  
A. Cevese ◽  
R. Grasso ◽  
R. Poltronieri ◽  
F. Schena
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Low Frequency ◽  
Peripheral Vascular Resistance ◽  
Common Mechanism ◽  
Peripheral Vascular ◽  
Frequency Range ◽  
Frequency Bands ◽  
Low Frequency Oscillations

The spontaneous variability of heart rate and arterial blood pressure was investigated in chloralose-anesthetized dogs with the left iliac vascular bed mechanically uncoupled from the central circulation. Electrocardiogram, mean arterial pressure (ABP), iliac perfusion and venous pressures, and flow (FLOW) were recorded for 5 min in steady state. Autoregressive spectral and cross-spectral analyses and digital filtering were performed. The variation coefficient (VC%), calculated from the overall variance of each signal, was 5–7%, with the exception of perfusion pressure (VC% = 1%). The frequency-related percentage of total variance was distributed among three frequency bands: two were < 0.20 Hz [lower (F1) and higher (F2; low-frequency range = F1 + F2)], and one was > 0.20 Hz (respiratory, F3). F3 was not always present in RR, which, however, oscillated also in F1 and F2, although with limited amplitude; ABP showed large respiratory and low-frequency oscillations; the FLOW oscillations were in the low-frequency range. Cross-spectral analysis showed high squared coherence in the relevant frequency bands between variables in the three couples: RR-ABP, RR-FLOW, and ABP-FLOW. Changes in RR preceded changes in ABP and in FLOW by > or = 3 s, whereas FLOW was approximately in phase opposition to ABP. It was concluded that, in the chloralose-anesthetized dog, 1) arterial pressure and heart rate oscillate with frequencies corresponding to those described in conscious humans, 2) low-frequency arterial pressure oscillations are due to changes in peripheral vascular resistance, and 3) peripheral vascular resistance does not display respiratory oscillations. Furthermore it was suggested that oscillations of vasomotor tone are generated by a rhythm of central origin and that F1 and F2 oscillations may recognize a common mechanism.

scholarly journals Estimation of Delay Times in Coupling Between Autonomic Regulatory Loops of Human Heart Rate and Blood Flow Using Phase Dynamics Analysis

2017 ◽  
Vol 9 (1) ◽  
pp. 16-22 ◽  
Author(s):  
Vladimir S Khorev ◽  
Anatoly S Karavaev ◽  
Elena E Lapsheva ◽  
Tatyana A Galushko ◽  
Mikhail D Prokhorov ◽  
...  
Keyword(s):  
Heart Rate ◽  
Delay Time ◽  
Healthy Subjects ◽  
Low Frequency ◽  
Phase Dynamics ◽  
Oscillatory Systems ◽  
Low Frequency Oscillations ◽  
Delay Times ◽  
The Difference ◽  
Regulatory Loop

Objective: We assessed the delay times in the interaction between the autonomic regulatory loop of Heart Rate Variability (HRV) and autonomic regulatory loop of photoplethysmographic waveform variability (PPGV), showing low-frequency oscillations. Material and Methods: In eight healthy subjects aged 25–30 years (3 male, 5 female), we studied at rest (in a supine position) the simultaneously recorded two-hour signals of RR intervals (RRIs) chain and finger photoplethysmogram (PPG). To extract the low-frequency components of RRIs and PPG signal, associated with the low-frequency oscillations in HRV and PPGV with a frequency of about 0.1 Hz, we filtered RRIs and PPG with a bandpass 0.05-0.15 Hz filter. We used a method for the detection of coupling between oscillatory systems, based on the construction of predictive models of instantaneous phase dynamics, for the estimation of delay times in the interaction between the studied regulatory loops. Results: Averaged value of delay time in coupling from the regulatory loop of HRV to the loop of PPGV was 0.9±0.4 seconds (mean ± standard error of the means) and averaged value of delay time in coupling from PPGV to HRV was 4.1±1.1 seconds. Conclusion: Analysis of two-hour experimental time series of healthy subjects revealed the presence of delay times in the interaction between regulatory loops of HRV and PPGV. Estimated delay time in coupling regulatory loops from HRV to PPGV was about one second or even less, while the delay time in coupling from PPGV to HRV was about several seconds. The difference in delay times is explained by the fact that PPGV to HRV response is mediated through the autonomic nervous system (baroreflex), while the HRV to PPGV response is mediated mechanically via cardiac output.

Reflexes from isolated carotid sinuses of intact and vagotomized conscious dogs

1980 ◽  
Vol 238 (6) ◽  
pp. H815-H822 ◽  
Author(s):  
R. B. Stephenson ◽  
D. E. Donald
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Response Curve ◽  
Vagal Afferents ◽  
Conscious Dogs ◽  
Stimulus Response ◽  
Carotid Baroreflex ◽  
Cervical Vagotomy ◽  
Curve Upward ◽  
Sinus Pressure

Exposure of the vascularly isolated carotid sinuses of 8 conscious dogs to static pressures between 50 and 240 mmHg caused significantly smaller increases [23 +/- 5(SE) mmHg] than decreases (37 +/- 4 mmHg) in arterial pressure frossure and heart rate and shifted the stimulus-response curve upward. Bilateral cervical vagotomy in conscious dogs caused sustained (3 h) increases in arterial pressure (40 +/- 5 mmHg), significantly larger than after atropinization (7 +/- 2 mmHg). In anesthetized, but not in conscious dogs, high sinus pressure reversed the hypertension caused by vagotomy. After vagotomy, low sinus pressure resulted in arterial pressures greater than 200 -mHg. In conscious dogs the carotid baroreflex can widely vary arterial pressure and heart rate despite buffering by extracarotid baroreceptors with vagal afferents, but cannot fully compensate for the acute loss of the latter. Extracarotid baroreceptors actively participate with carotid baroreceptors in the regulation of arterial pressure and better buffer carotid baroreflex-induced increases than decreases in arterial pressure.

Compensation to exsanguination hypotension in healthy conscious dogs

1963 ◽  
Vol 205 (5) ◽  
pp. 1000-1004 ◽  
Author(s):  
Robert F. Rushmer ◽  
Nolan Watson ◽  
Donald Harding ◽  
Donald Baker
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Human Subjects ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Systemic Arterial Pressure ◽  
Conscious Dogs ◽  
Series Of Experiments ◽  
The Mean ◽  
The Right

In some earlier studies on exsanguination hypotension in conscious dogs, reduction in systemic arterial pressure to shock levels was accompanied by a transient tachycardia during the removal of blood, but the heart rate returned to level, at or near control values during extended periods with the mean arterial pressure between 40 and 60 mm Hg. This observation stimulated a series of experiments on five healthy conscious dogs in which transient hypotension was induced by withdrawing blood from the region of the right atrium to determine which mechanisms were dominant in the compensatory reaction. A surprising degree of variability in response was encountered, such that tachycardia was the main response on some occasions, increased peripheral resistance on others, and in still others, several mechanisms appeared to play a role. Similar variability in the response to exsanguination have been reported in human subjects. These observations suggest that the baroceptor reflexes are not simple servo controls and their role in everyday cardiovascular responses should be re-examined.

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