scholarly journals Dissection of carotid sinus hypersensitivity: the timing of vagal and vasodepressor effects and the effect of body position

2011 ◽  
Vol 121 (9) ◽  
pp. 389-396 ◽  
Author(s):  
C. T. Paul Krediet ◽  
David L. Jardine ◽  
Wouter Wieling
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Sympathetic Nerve Activity ◽  
Carotid Sinus ◽  
Body Position ◽  
Muscle Sympathetic Nerve Activity ◽  
Peripheral Resistance ◽  
Head Up Tilt

We assessed the timing of vagal and sympathetic factors that mediate hypotension during CSM (carotid sinus massage) in patients with carotid sinus hypersensitivity. We hypothesized that a fall in cardiac output would precede vasodepression, and that vasodepression would be exaggerated by head-up tilt. We performed pulse contour analyses on blood pressure recordings during CSM in syncope patients during supine rest and head-up tilt. In a subset we simultaneously recorded muscle sympathetic nerve activity supine. During supine rest, systolic blood pressure decreased from 150±7 to 107±7 mmHg (P<0.001) and heart rate from 64±2 to 39±3 beats/min (P<0.01). Cardiac output decreased with heart rate to nadir (66±6% of baseline), 3.1±0.4 s after onset of bradycardia. In contrast, total peripheral resistance reached nadir (77±3% of baseline) after 11±1 s. During head-up-tilt, systolic blood pressure fell from 149±10 to 90±11 mmHg and heart rate decreased from 73±4 to 60±7 beats/min. Compared with supine rest, cardiac output nadir was lower (60±8 compared with 83±4%, P<0.05), whereas total peripheral resistance nadir was similar (81±6 compared with 80±3%). The time to nadir from the onset of bradycardia did not differ from supine rest. At the onset of bradycardia there was an immediate withdrawal of muscle-sympathetic nerve activity while total peripheral resistance decay occurred much later (6–8 s). The haemodynamic changes following CSM have a distinct temporal pattern that is characterized by an initial fall in cardiac output (driven by heart rate), followed by a later fall in total peripheral resistance, even though sympathetic withdrawal is immediate. This pattern is independent of body position.

Pet CO2 inversely affects MSNA response to orthostatic stress

2001 ◽  
Vol 281 (3) ◽  
pp. H1040-H1046 ◽  
Author(s):  
J. Kevin Shoemaker ◽  
Debbie D. O'Leary ◽  
Richard L. Hughson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Orthostatic Intolerance ◽  
Muscle Sympathetic Nerve Activity ◽  
Peripheral Resistance ◽  
Burst Frequency ◽  
Head Up Tilt ◽  
End Tidal ◽  
Combined Data

Arterial hypocapnia has been associated with orthostatic intolerance. Therefore, we tested the hypothesis that hypocapnia may be detrimental to increases in muscle sympathetic nerve activity (MSNA) and total peripheral resistance (TPR) during head-up tilt (HUT). Ventilation was increased ∼1.5 times above baseline for each of three conditions, whereas end-tidal Pco 2 (Pet CO2 ) was clamped at normocapnic (Normo), hypercapnic (Hyper; +5 mmHg relative to Normo), and hypocapnic (Hypo; −5 mmHg relative to Normo) conditions. MSNA (microneurography), heart rate, blood pressure (BP, Finapres), and cardiac output (Q, Doppler) were measured continuously during supine rest and 45° HUT. The increase in heart rate when changing from supine to HUT ( P < 0.001) was not different across Pet CO2 conditions. MSNA burst frequency increased similarly with HUT in all conditions ( P < 0.05). However, total MSNA and the increase in total amplitude relative to baseline (%ΔMSNA) increased more when changing to HUT during Hypo compared with Hyper ( P < 0.05). Both BP and Q were higher during Hyper than both Normo and Hypo (main effect; P < 0.05). Therefore, the MSNA response to HUT varied inversely with levels of Pet CO2 . The combined data suggest that augmented cardiac output with hypercapnia sustained blood pressure during HUT leading to a diminished sympathetic response.

Effect of sympathetic blockade on diurnal variation of hemodynamic patterns

1989 ◽  
Vol 256 (3) ◽  
pp. R778-R785 ◽  
Author(s):  
M. I. Talan ◽  
B. T. Engel
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Base Line ◽  
Sympathetic Blockade ◽  
Selective Blockade ◽  
Arterial Blood

Heart rate, stroke volume, and intra-arterial blood pressure were monitored continuously in each of four monkeys, 18 consecutive h/day for several weeks. The mean heart rate, stroke volume, cardiac output, systolic and diastolic blood pressure, and total peripheral resistance were calculated for each minute and reduced to hourly means. After base-line data were collected for approximately 20 days, observation was continued for equal periods of time under conditions of alpha-sympathetic blockade, beta-sympathetic blockade, and double sympathetic blockade. This was achieved by intra-arterial infusion of prazosin, atenolol, or a combination of both in concentration sufficient for at least 75% reduction of response to injection of agonists. The results confirmed previous findings of a diurnal pattern characterized by a fall in cardiac output and a rise in total peripheral resistance throughout the night. This pattern was not eliminated by selective blockade, of alpha- or beta-sympathetic receptors or by double sympathetic blockade; in fact, it was exacerbated by sympathetic blockade, indicating that the sympathetic nervous system attenuates these events. Because these findings indicate that blood volume redistribution is probably not the mechanism mediating the observed effects, we have hypothesized that a diurnal loss in plasma volume may mediate the fall in cardiac output and that the rise in total peripheral resistance reflects a homeostatic regulation of arterial pressure.

Carotid baroreceptor control of liver and spleen volume in cats

1991 ◽  
Vol 260 (1) ◽  
pp. H254-H259
Author(s):  
R. Maass-Moreno ◽  
C. F. Rothe
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Total Peripheral Resistance ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Normal Brain ◽  
Spleen Volume ◽  
Arterial Blood

We tested the hypothesis that the blood volumes of the spleen and liver of cats are reflexly controlled by the carotid sinus (CS) baroreceptors. In pentobarbital-anesthetized cats the CS area was isolated and perfused so that intracarotid pressure (Pcs) could be controlled while maintaining a normal brain blood perfusion. The volume changes of the liver and spleen were estimated by measuring their thickness using ultrasonic techniques. Cardiac output, systemic arterial blood pressure (Psa), central venous pressure, central blood volume, total peripheral resistance, and heart rate were also measured. In vagotomized cats, increasing Pcs by 100 mmHg caused a significant reduction in Psa (-67.8%), cardiac output (-26.6%), total peripheral resistance (-49.5%), and heart rate (-15%) and significantly increased spleen volume (9.7%, corresponding to a 2.1 +/- 0.5 mm increase in thickness). The liver volume decreased, but only by 1.6% (0.6 +/- 0.2 mm decrease in thickness), a change opposite that observed in the spleen. The changes in cardiovascular variables and in spleen volume suggest that the animals had functioning reflexes. These results indicate that in pentobarbital-anesthetized cats the carotid baroreceptors affect the volume of the spleen but not the liver and suggest that, although the spleen has an active role in the control of arterial blood pressure in the cat, the liver does not.

Decrease in cardiac output and muscle sympathetic activity during vasovagal syncope

2002 ◽  
Vol 282 (5) ◽  
pp. H1804-H1809 ◽  
Author(s):  
D. L. Jardine ◽  
I. C. Melton ◽  
I. G. Crozier ◽  
S. English ◽  
S. I. Bennett ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Sympathetic Nerve Activity ◽  
Vasovagal Syncope ◽  
Peripheral Resistance ◽  
Blood Pressure Level ◽  
Progressive Decline ◽  
Vasovagal Reactions ◽  
Head Up Tilt ◽  
Regression Slopes

The importance of cardiac output (CO) to blood pressure level during vasovagal syncope is unknown. We measured thermodilution CO, mean blood pressure (MBP), and leg muscle mean sympathetic nerve activity (MSNA) each minute during 60° head-up tilt in 26 patients with recurrent syncope. Eight patients tolerated tilt (TT) for 45 min (mean age 60 ± 5 yr) and 15 patients developed syncope during tilt (TS) (mean age 58 ± 4 yr, mean tilt time 15.4 ± 2 min). In TT patients, CO decreased during the first minute of tilt (from 3.2 ± 0.2 to 2.5 ± 0.3 l · min−1 · m−2, P = 0.001) and thereafter remained stable between 2.5 ± 0.3 ( P = 0.001) and 2.4 ± 0.2 l · min−1 · m−2( P = 0.004) at 5 and 45 min, respectively. In TS patients, CO decreased during the first minute (from 3.3 ± 0.2 to 2.7 ± 0.1 l · min−1 · m−2, P = 0.02) and was stable until 7 min before syncope, falling to 2.0 ± 0.2 at syncope ( P = 0.001). Regression slopes for CO versus time during tilt were −0.01 min−1 in TT versus −0.1 l · min−1 · m−2 · min−1in TS ( P = 0.001). However, MBP was more closely correlated to total peripheral resistance ( R = 0.56, P = 0.001) and MSNA ( R = 0.58, P = 0.001) than CO ( R = 0.32, P = 0.001). In vasovagal reactions, a progressive decline in CO may contribute to hypotension some minutes before syncope occurs.

Autonomic Cardiovascular Dysregulation at Rest and During Stress in Chronically Low Blood Pressure

2019 ◽  
Vol 33 (1) ◽  
pp. 39-53 ◽  
Author(s):  
Stefan Duschek ◽  
Alexandra Hoffmann ◽  
Casandra I. Montoro ◽  
Gustavo A. Reyes del Paso
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Baroreflex Sensitivity ◽  
Peripheral Resistance ◽  
Control Group ◽  
Low Blood Pressure

Abstract. Chronic low blood pressure (hypotension) is accompanied by symptoms such as fatigue, reduced drive, faintness, dizziness, cold limbs, and concentration difficulties. The study explored the involvement of aberrances in autonomic cardiovascular control in the origin of this condition. In 40 hypotensive and 40 normotensive subjects, impedance cardiography, electrocardiography, and continuous blood pressure recordings were performed at rest and during stress induced by mental calculation. Parameters of cardiac sympathetic control (i.e., stroke volume, cardiac output, pre-ejection period, total peripheral resistance), parasympathetic control (i.e., heart rate variability), and baroreflex function (i.e., baroreflex sensitivity) were obtained. The hypotensive group exhibited markedly lower stroke volume, heart rate, and cardiac output, as well as higher pre-ejection period and baroreflex sensitivity than the control group. Hypotension was furthermore associated with a smaller blood pressure response during stress. No group differences arose in total peripheral resistance and heart rate variability. While reduced beta-adrenergic myocardial drive seems to constitute the principal feature of the autonomic impairment that characterizes chronic hypotension, baroreflex-related mechanisms may also contribute to this state. Insufficient organ perfusion due to reduced cardiac output and deficient cardiovascular adjustment to situational requirements may be involved in the manifestation of bodily and mental symptoms.

Cardiovascular effects produced by L-glutamate stimulation of the lateral hypothalamic area

1989 ◽  
Vol 257 (2) ◽  
pp. H540-H552 ◽  
Author(s):  
S. E. Spencer ◽  
W. B. Sawyer ◽  
A. D. Loewy
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Lateral Hypothalamic Area ◽  
Hypothalamic Area ◽  
Pharmacological Blockade ◽  
Stimulation Of

L-Glutamate microinjections into the tuberal region of the lateral hypothalamic area (LHAt) caused a fall in blood pressure and heart rate in pentobarbital-anesthetized rats. The bradycardia was mediated by both beta-adrenergic and muscarinic mechanisms as demonstrated with pharmacological blockade. The hypotension was due to a decrease in cardiac output, not a decrease in total peripheral resistance. In addition, there was a reduction in coronary blood flow. If heart rate was held constant by pharmacological blockade or by electrical cardiac pacing, L-glutamate stimulation of the LHAt still caused a fall in blood pressure. When the electrically paced model was used, this hypotension was due to a fall in cardiac output. In contrast, with the pharmacological blockade of the heart, the hypotension was due to a decrease in the total peripheral resistance. The cardiac output reduction in the paced condition was not mediated solely by either beta-sympathetic or parasympathetic mechanisms as determined by pharmacological blockade. With heart rate held constant by either drugs or pacing, LHAt stimulation did not alter regional blood flow or resistance in any vascular bed, including the coronary circulation. We conclude that L-glutamate stimulation of the LHAt lowers the cardiac output and heart rate by both parasympathetic and beta-adrenergic mechanisms and elicits hypotension by lowering cardiac output in the naive and electrically paced model.

Nitric oxide synthase inhibition does not affect regulation of muscle sympathetic nerve activity during head-up tilt

2003 ◽  
Vol 285 (5) ◽  
pp. H2105-H2110 ◽  
Author(s):  
Jian Cui ◽  
Rong Zhang ◽  
Thad E. Wilson ◽  
Sarah Witkowski ◽  
Craig G. Crandall ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Heart Rate ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Total Activity ◽  
No Synthase ◽  
Sympathetic Outflow ◽  
Nerve Activity ◽  
Head Up Tilt

To test the hypothesis that systemic inhibition of nitric oxide (NO) synthase does not alter the regulation of sympathetic outflow during head-up tilt in humans, in eight healthy subjects NO synthase was blocked by intravenous infusion of NG-monomethyl-l-arginine (l-NMMA). Blood pressure, heart rate, cardiac output, total peripheral resistance (TPR), and muscle sympathetic nerve activity (MSNA) were recorded in the supine position and during 60° head-up tilt. In the supine position, infusion of l-NMMA increased blood pressure, via increased TPR, and inhibited MSNA. However, the increase in MSNA evoked by head-up tilt during l-NMMA infusion (change in burst rate: 24 ± 4 bursts/min; change in total activity: 209 ± 36 U/min) was similar to that during head-up tilt without l-NMMA (change in burst rate: 23 ± 4 bursts/min; change in total activity: 251 ± 52 U/min, n = 6, all P > 0.05). Moreover, changes in TPR and heart rate during head-up tilt were virtually identical between the two conditions. These results suggest that systemic inhibition of NO synthase with l-NMMA does not affect the regulation of sympathetic outflow and vascular resistance during head-up tilt in humans.

Hemodynamic Effects of "San-Huang-Hsieh-Hsin-Tang" in Patients with Essential Hypertension

1986 ◽  
Vol 14 (03n04) ◽  
pp. 153-156 ◽  
Author(s):  
Ho-Chan Chen ◽  
Ming-Tsuen Hsieh
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Essential Hypertension ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Contractile Force ◽  
Hemodynamic Effects ◽  
Cardiac Contractile ◽  
The Ancient Chinese

The ancient Chinese formula of "San-Huang-Hsieh-Hsin-Tang" (S-T) was originally used for patients with "epigastric fullness, flushing, restlessness, constipation and a hard pulse" (Chang 115 B.C.). All these symptoms are frequently observed in patients with essential hypertension. We assessed the antihypertensive and hemodynamic effects of this formula, and found that S-T decreased blood pressure, total peripheral resistance, heart rate and cardiac contractile force. S-T had no apparent effects on cardiac output and blood volume.

Assessing static and dynamic sympathetic transduction using microneurography

2021 ◽  
Author(s):  
Michael M. Tymko ◽  
Lindsey F. Berthelsen ◽  
Rachel J. Skow ◽  
Andrew R. Steele ◽  
Graham M. Fraser ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Peripheral Resistance ◽  
Analytical Techniques ◽  
Nerve Activity ◽  
Physiological Outcomes

The relationship between sympathetic nerve activity and the vasculature has been of great interest due to its potential role in various cardiovascular-related disease. This relationship, termed "sympathetic transduction", has been quantified using several different laboratory and analytical techniques. The most common method is to assess the association between relative changes in muscle sympathetic nerve activity, measured via microneurography, and physiological outcomes (e.g., blood pressure, total peripheral resistance, and blood flow etc.) in response to a sympathetic stressor (e.g. exercise, cold stress, orthostatic stress). This approach, however, comes with its own caveats. For instance, elevations in blood pressure and heart rate during a sympathetic stressor can have an independent impact on muscle sympathetic nerve activity. Another assessment of sympathetic transduction was developed by Wallin and Nerhed in 1982, where alterations in blood pressure and heart rate were assessed immediately following bursts of muscle sympathetic nerve activity at rest. This approach has since been characterized and further innovated by others, including the breakdown of consecutive burst sequences (e.g., singlet, doublet, triplet, and quadruplet), and burst height (quartile analysis) on specific vascular outcomes (e.g., blood pressure, blood flow, vascular resistance). The purpose of this review is to provide an overview of the literature that has assessed sympathetic transduction using microneurography and various sympathetic stressors (static sympathetic transduction) and using the same or similar approach established by Wallin and Nerhed at rest (dynamic neurovascular transduction). Herein, we discuss the overlapping literature between these two methodologies and highlight the key physiological questions that remain.

scholarly journals Fructose ingestion acutely elevates blood pressure in healthy young humans

2008 ◽  
Vol 294 (3) ◽  
pp. R730-R737 ◽  
Author(s):  
Clive M. Brown ◽  
Abdul G. Dulloo ◽  
Gayathri Yepuri ◽  
Jean-Pierre Montani
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Energy Expenditure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Health Concern ◽  
Arterial Blood ◽  
Glucose Ingestion

Overconsumption of fructose, particularly in the form of soft drinks, is increasingly recognized as a public health concern. The acute cardiovascular responses to ingesting fructose have not, however, been well-studied in humans. In this randomized crossover study, we compared cardiovascular autonomic regulation after ingesting water and drinks containing either glucose or fructose in 15 healthy volunteers (aged 21–33 yr). The total volume of each drink was 500 ml, and the sugar content 60 g. For 30 min before and 2 h after each drink, we recorded beat-to-beat heart rate, arterial blood pressure, and cardiac output. Energy expenditure was determined on a minute-by-minute basis. Ingesting the fructose drink significantly increased blood pressure, heart rate, and cardiac output but not total peripheral resistance. Glucose ingestion resulted in a significantly greater increase in cardiac output than fructose but no change in blood pressure and a concomitant decrease in total peripheral resistance. Ingesting glucose and fructose, but not water, significantly increased blood pressure variability and decreased cardiovagal baroreflex sensitivity. Energy expenditure increased by a similar amount after glucose and fructose ingestion, but fructose elicited a significantly greater increase in respiratory quotient. These results show that ingestion of glucose and fructose drinks is characterized by specific hemodynamic responses. In particular, fructose ingestion elicits an increase in blood pressure that is probably mediated by an increase in cardiac output without compensatory peripheral vasodilatation.

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