Identification of the Total Peripheral Resistance Baroreflex Impulse Response from Spontaneous Hemodynamic Variability: Validation by Chronic Arterial Baroreceptor Denervation

We previously developed a mathematical analysis technique for estimating the static gain values of the arterial total peripheral resistance (TPR) baroreflex ( GA) and the cardiopulmonary TPR baroreflex ( GC) from small, spontaneous beat-to-beat fluctuations in arterial blood pressure, cardiac output, and stroke volume. Here, we extended the mathematical analysis so as to also estimate the entire arterial TPR baroreflex impulse response [ hA( t)] as well as the lumped arterial compliance (AC). The extended technique may therefore provide a linear dynamic characterization of TPR baroreflex systems during normal physiological conditions from potentially noninvasive measurements. We theoretically evaluated the technique with respect to realistic spontaneous hemodynamic variability generated by a cardiovascular simulator with known system properties. Our results showed that the technique reliably estimated hA( t) [error = 30.2 ± 2.6% for the square root of energy ( EA), 19.7 ± 1.6% for absolute peak amplitude ( PA), 37.3 ± 2.5% for GA, and 33.1 ± 4.9% for the overall time constant] and AC (error = 17.6 ± 4.2%) under various simulator parameter values and reliably tracked changes in GC. We also experimentally evaluated the technique with respect to spontaneous hemodynamic variability measured from seven conscious dogs before and after chronic arterial baroreceptor denervation. Our results showed that the technique correctly predicted the abolishment of hA( t) [ EA = 1.0 ± 0.2 to 0.3 ± 0.1, PA = 0.3 ± 0.1 to 0.1 ± 0.0 s−1, and GA = −2.1 ± 0.6 to 0.3 ± 0.2 ( P < 0.05)] and the enhancement of GC [−0.7 ± 0.44 to −1.8 ± 0.2 ( P < 0.05)] following the chronic intervention. Moreover, the technique yielded estimates whose values were consistent with those reported with more invasive and/or experimentally difficult methods.

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Role of arterial baroreceptors in mediating cardiovascular response to exercise

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1976.230.1.85 ◽

1976 ◽

Vol 230 (1) ◽

pp. 85-89 ◽

Cited By ~ 35

Author(s):

RJ McRitchie ◽

SF Vatner ◽

D Boettcher ◽

GR Heyndrickx ◽

TA Patrick ◽

...

Keyword(s):

Heart Rate ◽

Cardiac Output ◽

Total Peripheral Resistance ◽

Cardiovascular Response ◽

Peripheral Resistance ◽

Aortic Pressure ◽

Severe Exercise ◽

Response To Exercise ◽

Arterial Baroreceptor

The role played by the major arterial baroreceptor reflexes in the cardiovascular response to exercise was examined by comparing the responses of untethered conscious dogs instrumented for the measurement of aortic pressure and cardiac output with those of dogs with total arterial barorecptor denervation (TABD). Moderately severe levels of exercise (12 mph) in intact dogs increased cardiac output from 111 +/- 17 ml/kg per min, increased heart rate from 101 +/- 5 to 265 +/- 8 beats/min, and reduced total peripheral resistance from 0.039 +/- 0.003 to 0.015 +/- 0.002 mmHg/ml per min. Dogs with TABD responded in a very similar fashion; exercise increased cardiac output from 119 +/- 8 to 356 /+- 23 ml/kg per min, increased heart rate from 122 +/- 7 to 256 +/- 5 beats/min, and decreased total peripheral resistance from 0.042 +/- 0.005 to +/- 0.015 +/- 0.001 mmHg/ml per min. The reflex heart rate responses to intravenous bolus doses of methoxamine were also examined in intact animals, both at rest and during exercise. Methoxamine caused striking bradycardia at rest, but little bradycardia during exercise. These results suggest that the arterial baroreceptor reflex is normally turned off during severe exercise and thus does not modify significantly the cardiovascular response to exercise.

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Estimation of arterial and cardiopulmonary total peripheral resistance baroreflex gain values: validation by chronic arterial baroreceptor denervation

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00898.2005 ◽

2006 ◽

Vol 290 (5) ◽

pp. H1830-H1836 ◽

Cited By ~ 16

Author(s):

Ramakrishna Mukkamala ◽

Jong-Kyung Kim ◽

Ying Li ◽

Javier Sala-Mercado ◽

Robert L. Hammond ◽

...

Keyword(s):

Blood Pressure ◽

Total Peripheral Resistance ◽

Experimental Testing ◽

Peripheral Resistance ◽

Noninvasive Technique ◽

Baroreflex Control ◽

Arterial Blood ◽

Cardiopulmonary Baroreflex ◽

Reflex Control ◽

Arterial Baroreceptor

Feedback control of total peripheral resistance (TPR) by the arterial and cardiopulmonary baroreflex systems is an important mechanism for short-term blood pressure regulation. Existing methods for measuring this TPR baroreflex mechanism typically aim to quantify only the gain value of one baroreflex system as it operates in open-loop conditions. As a result, the normal, integrated functioning of the arterial and cardiopulmonary baroreflex control of TPR remains to be fully elucidated. To this end, the laboratory of Mukkamala et al. (Mukkamala R, Toska K, and Cohen RJ. Am J Physiol Heart Circ Physiol 284: H947–H959, 2003) previously proposed a potentially noninvasive technique for estimating the closed-loop (dimensionless) gain values of the arterial TPR baroreflex (GA) and the cardiopulmonary TPR baroreflex (GC) by mathematical analysis of the subtle, beat-to-beat fluctuations in arterial blood pressure, cardiac output, and stroke volume. Here, we review the technique with additional details and describe its experimental evaluation with respect to spontaneous hemodynamic variability measured from seven conscious dogs, before and after chronic arterial baroreceptor denervation. The technique was able to correctly predict the group-average changes in GA and GC that have previously been shown to occur following chronic arterial baroreceptor denervation. That is, reflex control by the arterial TPR baroreflex was virtually abolished (GA = −2.1 ± 0.6 to 0.3 ± 0.2; P < 0.05), while reflex control by the cardiopulmonary TPR baroreflex more than doubled (GC = −0.7 ± 0.4 to −1.8 ± 0.2; P < 0.05). With further successful experimental testing, the technique may ultimately be employed to advance the basic understanding of TPR baroreflex functioning in both humans and animals in health and disease.

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Diastolic pressure and peripheral resistance during stellate ganglion stimulation

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1963.204.1.71 ◽

1963 ◽

Vol 204 (1) ◽

pp. 71-72 ◽

Cited By ~ 1

Author(s):

Edward D. Freis ◽

Jay N. Cohn ◽

Thomas E. Liptak ◽

Aristide G. B. Kovach

Keyword(s):

Heart Rate ◽

Blood Flow ◽

Cardiac Output ◽

Total Peripheral Resistance ◽

Diastolic Pressure ◽

Stellate Ganglion ◽

Peripheral Resistance ◽

Resistance Vessels ◽

Left Stellate Ganglion ◽

Increased Blood Flow

The mechanism of the diastolic pressure elevation occurring during left stellate ganglion stimulation was investigated. The cardiac output rose considerably, the heart rate remained essentially unchanged, and the total peripheral resistance fell moderately. The diastolic rise appeared to be due to increased blood flow rather than to any active changes in resistance vessels.

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Elevated Blood Pressure in Adolescence Is Attributable to a Combination of Elevated Cardiac Output and Total Peripheral Resistance

Hypertension ◽

10.1161/hypertensionaha.118.11925 ◽

2018 ◽

Vol 72 (5) ◽

pp. 1103-1108 ◽

Cited By ~ 6

Author(s):

Chloe Park ◽

Abigail Fraser ◽

Laura D. Howe ◽

Siana Jones ◽

George Davey Smith ◽

...

Keyword(s):

Blood Pressure ◽

Cardiac Output ◽

Total Peripheral Resistance ◽

Peripheral Resistance ◽

Elevated Blood Pressure ◽

Elevated Blood

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RSR-13, an allosteric effector of hemoglobin, increases systemic and iliac vascular resistance in rats

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1996.271.2.h602 ◽

1996 ◽

Vol 271 (2) ◽

pp. H602-H613 ◽

Cited By ~ 5

Author(s):

M. P. Kunert ◽

J. F. Liard ◽

D. J. Abraham

Keyword(s):

Cardiac Output ◽

Vascular Resistance ◽

Total Peripheral Resistance ◽

Peripheral Resistance ◽

Experimental Models ◽

Metabolic Demand ◽

Flow Probe ◽

Inositol Hexaphosphate ◽

Control Value ◽

Allosteric Effector

Tissue O2 delivery in excess of metabolic demand may be a factor in the development of high vascular resistance in experimental models of volume-expanded hypertension. This hypothesis was previously tested in rats with an exchange transfusion of red blood cells treated with inositol hexaphosphate or an intravenous infusion of RSR-4, allosteric effectors of hemoglobin. The binding of these drugs with hemoglobin effect a conformational change in the molecule, such that the affinity for O2 is reduced. However, in both preparations, the changes in vascular resistance could have been nonspecific. The present studies used intravenous infusions of RSR-13, which did not share some of the problematic characteristics of RSR-4 and inositol hexaphosphate. Conscious instrumented rats (an electromagnetic flow probe on ascending aorta or an iliac, mesenteric, or renal Doppler flow probe) were studied for 6 h after an RSR-13 infusion of 200 mg/kg in 15 min. This dose significantly increased arterial P50 (PO2 at which hemoglobin is 50% saturated) from 38 +/- 0.8 to 58 +/- 1.4 mmHg at 1 h after the start of the infusion. In the 3rd h cardiac output fell significantly from a control value of 358 +/- 33 to 243 +/- 24 ml.kg-1.min-1 and total peripheral resistance significantly increased from 0.31 +/- 0.03 to 0.43 +/- 0.04 mmHg.ml-1.kg.min. Cardiac output and P50 returned toward control over the next few hours. Neither cardiac output nor total peripheral resistance changed in the group of rats receiving vehicle alone. In a separate group of rats, iliac flow decreased significantly to 60% of control and iliac resistance increased to 160% of control. Iliac flow increased significantly in the group of rats that received vehicle only. Although the mechanism of these changes has not been established, these results suggest that a decreased O2 affinity leads to an increased total peripheral resistance and regional vascular resistance and support the hypothesis that O2 plays a role in the metabolic autoregulation of blood flow.

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Long-term hemodynamic actions of atrial natriuretic factor (99-126) in conscious sheep

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1988.254.4.h811 ◽

1988 ◽

Vol 254 (4) ◽

pp. H811-H815 ◽

Cited By ~ 4

Author(s):

D. G. Parkes ◽

J. P. Coghlan ◽

J. G. McDougall ◽

B. A. Scoggins

Keyword(s):

Blood Pressure ◽

Cardiac Output ◽

Stroke Volume ◽

Blood Volume ◽

Total Peripheral Resistance ◽

Atrial Natriuretic Factor ◽

Peripheral Resistance ◽

Natriuretic Factor ◽

Atrial Natriuretic

The hemodynamic and metabolic effects of long-term (5 day) infusion of human atrial natriuretic factor (ANF) were examined in conscious chronically instrumented sheep. Infusion of ANF at 20 micrograms/h, a rate below the threshold for an acute natriuretic effect, decreased blood pressure by 9 +/- 1 mmHg on day 5, associated with a fall in calculated total peripheral resistance. On day 1, ANF reduced cardiac output, stroke volume, and blood volume, effects that were associated with an increase in heart rate and calculated total peripheral resistance and a small decrease in blood pressure. On days 4 and 5 there was a small increase in urine volume and sodium excretion. On day 5 an increase in water intake and body weight was observed. No change was seen in plasma concentrations of renin, arginine vasopressin, glucose, adrenocorticotropic hormone, or protein. This study suggests that the short-term hypotensive effect of ANF results from a reduction in cardiac output associated with a fall in both stroke volume and effective blood volume. However, after 5 days of infusion, ANF lowers blood pressure via a reduction in total peripheral resistance.

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