Influence of acute alterations in heart rate and systemic arterial pressure on echocardiographic measures of left ventricular perfornmance in normal human subjects.

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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Diastolic pressure determines autonomic responses to pressure perturbation in humans

Journal of Applied Physiology ◽

10.1152/jappl.1989.66.2.800 ◽

1989 ◽

Vol 66 (2) ◽

pp. 800-807 ◽

Cited By ~ 25

Author(s):

J. S. Sanders ◽

D. W. Ferguson

Keyword(s):

Heart Rate ◽

Arterial Pressure ◽

Sympathetic Nerve Activity ◽

Diastolic Pressure ◽

Human Subjects ◽

Muscle Sympathetic Nerve Activity ◽

Venous Pressure ◽

Central Venous ◽

Nerve Activity ◽

Normal Human

Arterial baroreceptors reflexly regulate sympathetic and heart rate responses to alteration of blood pressure. The primary mechanical determinant of arterial baroreceptor activity in humans remains unclear. We examined the influence of systolic, diastolic, pulse, and mean arterial pressures on efferent muscle sympathetic nerve activity (MSNA, microneurography) and heart rate responses during perturbation of arterial pressure in 10 normal human subjects [age 25 +/- 2 (SE) yr]. We directly measured arterial pressure, heart rate, and MSNA during intravenous vasodilator infusion (nitroprusside, 6 +/- 1 micrograms.kg-1.min-1, n = 6; or hydralazine, 16 +/- 2 mg, n = 4) while central venous pressure was held constant by simultaneous volume expansion. Changes in arterial pressures were compared with changes in heart rate and MSNA over 3-min periods of vasodilator infusion during which we observed increases in systolic and pulse pressures with simultaneous decreases in mean and diastolic pressures. During vasodilator infusion, there were increases in systolic (124.2 +/- 2.1 to 131.7 +/- 2.9 Torr, P less than 0.001) and pulse pressures (57.0 +/- 2.2 to 72.7 +/- 2.7 Torr, P less than 0.001) although mean arterial pressure fell (88.0 +/- 2.6 to 80.4 +/- 2.7 Torr, P less than 0.001) because of decreases in diastolic pressure (67.2 +/- 3.0 to 59.0 +/- 2.7 Torr, P less than 0.001). The changes in arterial pressures were accompanied by simultaneous increases in heart rate (66.4 +/- 3.0 to 92.6 +/- 4.8 beats/min, P less than 0.001) and MSNA (327 +/- 59 to 936 +/- 171 U, P less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

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Effects of tocainide on left ventricular performance at rest and during acute alterations in heart rate and systemic arterial pressure. An echocardiographic study.

Heart ◽

10.1136/hrt.41.2.175 ◽

1979 ◽

Vol 41 (2) ◽

pp. 175-181 ◽

Cited By ~ 20

Author(s):

W F Ryan ◽

J S Karliner

Keyword(s):

Heart Rate ◽

Arterial Pressure ◽

Systemic Arterial Pressure ◽

Left Ventricular ◽

Left Ventricular Performance ◽

Ventricular Performance ◽

Echocardiographic Study

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Reflex sympathetic augmentation of left-ventricular inotropic state in the conscious dog

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1981.241.6.h857 ◽

1981 ◽

Vol 241 (6) ◽

pp. H857-H863

Author(s):

C. Yoran ◽

L. Higginson ◽

M. A. Romero ◽

J. W. Covell ◽

J. Ross

Keyword(s):

Heart Rate ◽

Arterial Pressure ◽

Pressure Rise ◽

Left Ventricular Pressure ◽

Systemic Arterial Pressure ◽

Left Ventricular ◽

Adrenergic Blockade ◽

Conscious Dog ◽

Inotropic State ◽

Simultaneous Decrease

Cardiac reflex responses to a series of partial inferior vena caval occlusions were studied in conscious previously instrumented dogs. Heart rate responses during the fall of systemic arterial pressure were mediated both by increased sympathetic tone and withdrawal of parasympathetic tone. Responses of the left-ventricular inotropic state, estimated from changes in left ventricular pressure rise (LV dP/dt), were studied early after release of a series of partial vena caval occlusions, and a positive linear relation between the prior fall in the systemic arterial pressure and the increase in LV dP/dt was demonstrated. Serial studies showed this effect of persist for at least 12 s beyond the reflex slowing of heart rate early after release of vena caval occlusion. The positive inotropic response was markedly attenuated by beta-adrenergic blockade and also occurred at a constant heart rate. It was present after adrenalectomy. These studies suggest that the integrated baroreceptor responses that are activated by a simultaneous decrease in the venous return and systemic arterial pressure play an important role in the regulation of left-ventricular inotropic state in the conscious dog.

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Faculty Opinions recommendation of The relative contribution of prosthetic gradients, systemic arterial pressure, and pulse pressure to the left ventricular pressure in patients with aortic prosthetic valves.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.9881957.10592055 ◽

2011 ◽

Author(s):

Olav F Münter Sellevold

Keyword(s):

Arterial Pressure ◽

Pulse Pressure ◽

Left Ventricular Pressure ◽

Systemic Arterial Pressure ◽

Left Ventricular ◽

Ventricular Pressure ◽

Relative Contribution ◽

Prosthetic Valves

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Nocturnal headache: systemic arterial pressure and heart rate during sleep

Cephalalgia ◽

10.1177/03331024830030s106 ◽

1983 ◽

Vol 3 (1_suppl) ◽

pp. 54-57 ◽

Cited By ~ 5

Author(s):

Fabio Cirignotta ◽

Giorgio Coccagna ◽

Tommaso Sacquegna ◽

Emiliana Sforza ◽

Giuseppe Lamontanara ◽

...

Keyword(s):

Heart Rate ◽

Arterial Pressure ◽

Rem Sleep ◽

Continuous Monitoring ◽

Systemic Arterial Pressure ◽

Fréquence Cardiaque ◽

The Awakening ◽

Sono Stati ◽

Autonomic Instability ◽

Polygraphic Recording

In order to evaluate autonomic nervous system changes occurring before nocturnal headache attacks, we studied three subjects (one male, two females) suffering from chronic migraine. All three patients underwent a nocturnal polygraphic recording including continuous monitoring of systemic arterial pressure and heart rate. Two subjects showed increases and irregularities of arterial pressure before awakening with headache. These changes began during N–REM sleep and lasted during REM sleep preceding the awakening with headache. Heart rate did not change before the attacks. These findings do not support the hypothesis that autonomic instability during REM sleep represents the precipitating factor of the attacks. On a étudié avec des méthodes polygrafiques trois sujets (1 homme et deux femmes) souffrant d'hémicranie chronique avec des crises nocturnes. Chez deux malades les crises étaient précédées d'augmentation et d'irrégularité de la tension artérielle. Ces modifications commençaient pendant le sommeil N-REM et contineaient pendant le sommeil REM qui précédait le réveil avec hémicranie. La fréquence cardiaque n'a pas subi de modification avant les crises. Les résultats obtenus ne confirment l'hypothèse selon laquelle le facteur causant les crises est l'instabilité anticronique à la fase REM. Sono stati studiati con metodiche poligrafiche 3 soggetti (1 maschio e 2 femmine) affetti da emicrania cronica con attacchi notturni. In 2 di essi gli attacchi erano preceduti da incrementi ed irregolarità della pressione arteriosa. Tali modificazioni iniziavano durante il sonno N-REM e perduravano nel corso del sonno REM che precedeva il risveglio con cefalea. La frequenza cardiaca non si modificava prima dell'attacco. I risultati ottenuti non confermano l'ipotesi che il fattore precipitante gli attacchi emicranici sia l'instabilità anticronica della fase REM.

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Regional blood volume distribution during positive and negative airway pressure breathing in supine humans

Journal of Applied Physiology ◽

10.1152/jappl.1993.75.4.1740 ◽

1993 ◽

Vol 75 (4) ◽

pp. 1740-1747 ◽

Cited By ~ 16

Author(s):

J. Peters ◽

B. Hecker ◽

D. Neuser ◽

W. Schaden

Keyword(s):

Heart Rate ◽

Blood Flow ◽

Arterial Pressure ◽

Vascular Resistance ◽

Airway Pressure ◽

Left Ventricular ◽

Whole Body ◽

Blood Content ◽

Calf Blood Flow ◽

Negative Airway Pressure

To assess the effects of continuous positive (CPAP) or negative airway pressure (CNAP) breathing (+/- 10#x2013;12 cmH2O, duration 25 min) on blood content in the body's capacitance vasculature, regional distribution of labeled red blood cells was evaluated in seven spontaneously breathing supine volunteers. Counts were acquired by whole body scans and detectors overlying the liver, intestine, left ventricle, and lower arm, and arterial pressure, heart rate, calf blood flow and vascular resistance, hematocrit, vasopressin, and atrial natriuretic peptide plasma concentrations were also obtained. With CPAP, thoracic, cardiac, and left ventricular counts diminished significantly by 7#x2013;10%, were accompanied by significant increases in counts over both the gut and liver, and remained decreased during CPAP but reversed to baseline with zero airway pressure. Calf blood flow and vascular resistance significantly decreased and increased, respectively, whereas limb counts, arterial pressure, heart rate, and hormone concentrations remained unchanged. With CNAP, in contrast, regional counts and other variables did not change. Thus, moderate levels of CPAP deplete the intrathoracic vascular bed and heart, shifting blood toward the gut and liver but not toward the limbs. No short-term compensation increasing cardiac filling during CPAP was seen. In contrast, CNAP did not alter intrathoracic or organ blood content and, therefore, does not simply mirror the effects evoked by CPAP.

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Arterial pressure-flow relations in the awake standing dog

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1975.229.5.1261 ◽

1975 ◽

Vol 229 (5) ◽

pp. 1261-1270 ◽

Cited By ~ 11

Author(s):

W Enrlich ◽

FV Schrijen ◽

TA Solomon ◽

E Rodriguez-Lopez ◽

RL Riley

Keyword(s):

Heart Rate ◽

Arterial Pressure ◽

Rate Increase ◽

Diastolic Pressure ◽

Aortic Pressure ◽

Left Ventricular ◽

Right Atrial ◽

Heart Rate Increase ◽

Underlying Mechanisms ◽

The Right

The transient circulatory changes following paced heart rate increase are reported from 133 trials with 6 unanesthetized dogs with chronically implanted monitoring devices for heart rate, cardiac output, aortic blood pressure, and mean right atrial pressure. In 62 trials with 2 of the dogs, pulmonary artery, and left ventricular end-diastolic pressure, as well as left ventricular dP/dt were also studied. The sequence of changes in pressures and flows is analyzed in terms of probable underlying mechanisms, particularly with respect to the nature of vascular resistances. The rise in aortic pressure and flow during the first 3 s of paced heart rate increase, before arterial stretch receptor reflexes become active, is more consistent with an effective downstream pressure of about 49 mmHg, presumably at the arteriolar level, than with an effective downstream pressure close to 0 mmHg at the right atrial level. In the pulmonary circulation where vascular reflex effects are less prominent, the pattern of pulmonary arterial pressure and flow for the entire 30 s of observation is consistent with an effective downstream pressure of 9 mmHg, presumably at the alveolar or pulmonary arteriolar level, rather than at the level of the left ventricular end-diastolic pressure.

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

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1987.253.6.h1477 ◽

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.

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Roles of right versus left vagal sensory nerves in cardiopulmonary reflexes of conscious dogs

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1985.249.3.r301 ◽

1985 ◽

Vol 249 (3) ◽

pp. R301-R307 ◽

Cited By ~ 1

Author(s):

K. W. Barron ◽

V. S. Bishop

Keyword(s):

Heart Rate ◽

Arterial Pressure ◽

Left Ventricular ◽

Sensory Nerves ◽

Inhibitory Influence ◽

Relative Pressure ◽

Intracoronary Administration ◽

The Right ◽

Vagal Sensory Nerves ◽

Change In Mean

This study examined the relative roles of the right vs. left vagi in mediating the inhibitory influence of vagal sensory input on sympathetic outflow to the cardiovascular system. This objective was pursued through examination of responses to 1) interruption of tonic vagal input and 2) intracoronary administration of veratridine (Bezold-Jarisch effect). Bilateral vagal cold block (BVB) (n = 16) increased arterial pressure 25 +/- 3 mmHg and heart rate 66 +/- 7 beat/min, whereas right vagal cold block (RVB) and left vagal cold block (LVB) increased arterial pressure 13 +/- 2 and 4 +/- 2 mmHg, respectively. The relative differences in the change in mean arterial pressure were independent of heart rate since similar changes in arterial pressure were observed with preelevation of heart rate with atropine. Sinoaortic baroreceptor denervation augmented the pressure responses approximately fourfold, with the relative pressure changes produced by BVB, RVB, or LVB remaining proportionally the same. Intracoronary administration of veratridine (0.1 g/kg) produced a hypotension action (-44 +/- 6 mmHg), bradycardia (-48 +/- 8 beat/min), and a negative intropic effect (-482 +/- 68 mmHg/s, left ventricular (LV) (dP/dt)max. During RVB the depressor effect of veratridine was reduced to -18 +/- 5 mmHg, and changes in heart rate or LV (dP/dt)max were abolished. Veratridine administration during LVB decreased arterial pressure (-39 +/- 6 mmHg), heart rate (-22 +/- 6 beat/min), and LV (dP/dt)max (-250 +/- 60 mmHg). We conclude that in the conscious dog the tonic inhibitory influence of vagal afferent nerves on vasomotor outflow is predominantly associated with the right vagus as in Bezold-Jarisch effect.

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