Altered heart rate-arterial pressure relation during head-out water immersion in conscious dog

1988 ◽  
Vol 254 (4) ◽  
pp. R595-R601 ◽  
Author(s):  
H. Yoshino ◽  
D. C. Curran-Everett ◽  
S. K. Hong ◽  
J. A. Krasney
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Inferior Vena ◽  
Water Immersion ◽  
Vena Cava ◽  
Systolic Arterial Pressure ◽  
Baroreflex Control ◽  
Rate Range ◽  
Average Gain ◽  
Cholinergic Regulation

The influence of head-out water immersion (WI) (37 degrees C) on baroreflex control of heart rate was studied in five trained, instrumented, conscious dogs. Arterial pressure was raised and lowered using occluder cuffs implanted around the aorta and inferior vena cava. Function curves relating transmural systolic arterial pressure (TSAP = systolic arterial pressure-pleural pressure) to heart rate (HR) were constructed to compare responses in air and during WI. The resting TSAP in air [142 +/- 8 mmHg (mean +/- SE) at 78 +/- 6 beats/min] increased significantly during WI (161 +/- 9 mmHg at 109 +/- 9 beats/min). During WI, the saturation TSAP at the bradycardia plateau of the relation increased significantly, by 19 mmHg, whereas the average gain (slope) of the relation decreased significantly, from -1.426 to -0.752 beats.min-1.mmHg-1. Therefore, WI elicits both a resetting and a decrease of the average gain of the TSAP-HR relation. The heart rate range increased during WI as well. After cholinergic blockade with atropine, WI did not elicit a resetting of the relation and the change in average gain was abolished. However, after beta 1-blockade with metoprolol, the resting TSAP increased significantly during WI and resetting persisted, but the decrease of average gain was abolished. Therefore, the alteration of the TSAP-HR relation in WI is achieved via a modulation of both adrenergic and cholinergic regulation of HR.

Comparison of phenylephrine bolus and infusion methods in baroreflex measurements

1990 ◽  
Vol 69 (3) ◽  
pp. 962-967 ◽  
Author(s):  
J. T. Sullebarger ◽  
C. S. Liang ◽  
P. D. Woolf ◽  
A. E. Willick ◽  
J. F. Richeson
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Baroreflex Sensitivity ◽  
Heart Rate Response ◽  
Pressor Response ◽  
Plasma Catecholamines ◽  
Systolic Arterial Pressure ◽  
Normal Subjects ◽  
Vagus Nerves ◽  
Baroreflex Control

Phenylephrine (PE) bolus and infusion methods have both been used to measure baroreflex sensitivity in humans. To determine whether the two methods produce the same values of baroreceptor sensitivity, we administered intravenous PE by both bolus injection and graded infusion methods to 17 normal subjects. Baroreflex sensitivity was determined from the slope of the linear relationship between the cardiac cycle length (R-R interval) and systolic arterial pressure. Both methods produced similar peak increases in arterial pressure and reproducible results of baroreflex sensitivity in the same subjects, but baroreflex slopes measured by the infusion method (9.9 +/- 0.7 ms/mmHg) were significantly lower than those measured by the bolus method (22.5 +/- 1.8 ms/mmHg, P less than 0.0001). Pretreatment with atropine abolished the heart rate response to PE given by both methods, whereas plasma catecholamines were affected by neither method of PE administration. Naloxone pretreatment exaggerated the pressor response to PE and increased plasma beta-endorphin response to PE infusion but had no effect on baroreflex sensitivity. Thus our results indicate that 1) activation of the baroreflex by the PE bolus and infusion methods, although reproducible, is not equivalent, 2) baroreflex-induced heart rate response to a gradual increase in pressure is less than that seen with a rapid rise, 3) in both methods, heart rate response is mediated by the vagus nerves, and 4) neither the sympathetic nervous system nor the endogenous opiate system has a significant role in mediating the baroreflex control of heart rate to a hypertensive stimulus in normal subjects.

Cardiovascular Effects of Vasopressin Infused into the Vertebral Circulation of Conscious Dogs

1981 ◽  
Vol 61 (3) ◽  
pp. 345-347 ◽  
Author(s):  
J. F. Liard ◽  
O. Dériaz ◽  
M. Tschopp ◽  
J. Schoun
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Inferior Vena ◽  
Vena Cava ◽  
Electromagnetic Flowmeter ◽  
Cardiovascular Effects ◽  
Conscious Dogs ◽  
Left Vertebral Artery ◽  
Plasma Vasopressin ◽  
The Central Nervous System

1. Seven conscious dogs received arginine-vasopressin infusions (100 and 1000 fmol min−1 kg−1) through catheters implanted in the left vertebral artery or the inferior vena cava while arterial pressure, cardiac output (electromagnetic flowmeter) and heart rate were measured. 2. Despite similar increases in plasma vasopressin concentrations, intravertebral administration induced a lesser increase in mean arterial pressure and a greater decrease in heart rate than the same infusion given intravenously. 3. These results suggest that vasopressin has an effect on structures of the central nervous system involved in cardiovascular control, possibly by affecting the baroreceptor reflex.

ARTERIAL AND VENOUS BLOOD PRESSURE RESPONSES DURING A REDUCTION IN BLOOD VOLUME AND HYPOXIA AND HYPERCAPNIA IN INFANTS DURING THE FIRST TWO DAYS OF LIFE

PEDIATRICS ◽  
1966 ◽  
Vol 37 (5) ◽  
pp. 733-742
Author(s):  
Maureen Young ◽  
Dennis Cottom
Keyword(s):  
Heart Rate ◽  
Inferior Vena Cava ◽  
Arterial Pressure ◽  
Blood Volume ◽  
Inferior Vena ◽  
Recovery Period ◽  
Vena Cava ◽  
Ductus Venosus ◽  
Volume Distribution ◽  
The Mean

In 46 normal full-term infants (0.5-36.5 hours of age) the mean systolic pressure in the lower aorta, catheterized through the umbilical artery, was 70 S.D. ± 8 mm Hg and the mean diastolic pressure 44 S.D. ± 7 mm Hg. The mean venous pressure in the thoracic inferior vena cava, catheterized through the umbilical vein and ductus venosus was 1.4 S.D. ± 2 cm H2O. Higher pressures were recorded in the portal sinus. The mean arterial O2 tension in the lower aorta was 84 S.D. ± 13 mm Hg and the mean CO2 tension 37 S.D. ± 7 mm Hg. The mean rectal temperature was 36.2 S.D. ± 0.7°C. Arterial pressure tracings recorded during, and in the recovery period following, a 10% reduction in blood volume suggest that vasomoter baroreceptor responses to a reduction in pulse pressure are not very active during the first 2 days of life. Cardiac responses are more active. In contrast to the adult, passive tipping of the newborn infant into the head-up position caused little change in the inferior vena cava pressure or in the arterial pressure. An increase in intratracheal pressure of 7-10 cm H2O caused immediate bradycardia. Frequently the heart rate was halved but little fall in mean pressure occurred over 10 seconds. Breathing hypoxic mixtures caused hypotension and tachycardia. Hypotension was observed with no change in heart rate when the arterial CO2 was raised simultaneously. Differences in blood volume distribution, and the relative size of the circulatory beds under reflex and chemical control, possibly share with the apparent unresponsiveness of the peripheral vessels in causing the differences in responses observed between the infant and the adult.

Altered heart rate baroreflex during pregnancy: role of sympathetic and parasympathetic nervous systems

1997 ◽  
Vol 273 (3) ◽  
pp. R960-R966 ◽  
Author(s):  
V. L. Brooks ◽  
C. M. Kane ◽  
D. M. Van Winkle
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Late Pregnancy ◽  
Baroreflex Control ◽  
Rate Range ◽  
Before And After ◽  
Reflex Gain ◽  
The Difference ◽  
Perfused Hearts

Two studies were performed to determine whether the attenuation of baroreflex control of heart rate during late pregnancy in conscious rabbits is due to changes in parasympathetic (Para) or sympathetic (Sym) control of the heart. In the first, baroreflex relationships between arterial pressure and heart rate were generated before and after treatment with propranolol (Pro) to block Sym or with methscopolamine (Meth) to block Para. Each rabbit was studied in both the pregnant and nonpregnant state. Pregnancy decreased maximum baroreflex gain from 14.9 +/- 4.0 to 4.8 +/- 0.9 beats.min-1.mmHg-1 (P < 0.01) and decreased heart rate range from 177 +/- 6 to 143 +/- 10 beats/min (P < 0.01), primarily by increasing minimum heart rate (114 +/- 6 to 134 +/- 8 beats/min; P < 0.01). The difference between pregnant and nonpregnant rabbits in baroreflex gain was not altered by Meth but was abolished by Pro, suggesting that it is due to decreased Sym control of the heart. The elevated minimum heart rate of pregnancy persisted after Pro, but was abolished by Meth, suggesting that it is mediated by decreased Para control of the heart. In the second study, isolated buffer-perfused hearts from pregnant and nonpregnant rabbits were treated with increasing doses of isoproterenol (0.3-300 mM) or acetylcholine (0.3-10,000 microM), and the heart rate responses were determined. Hearts from pregnant rabbits were more sensitive to isoproterenol (P < 0.05), but less responsive to acetylcholine (P < 0.05). In conclusion, pregnancy-induced decreases in cardiac reflex gain and range appear to be mediated by alterations in Sym and Para, respectively. The change in Sym occurs proximal to the heart, whereas the decreased contribution of Para may be due, at least in part, to decreased sensitivity of the heart to acetylcholine.

Compensatory recovery of parasympathetic control of heart rate after unilateral vagotomy in rabbits

1992 ◽  
Vol 262 (4) ◽  
pp. H1122-H1127 ◽  
Author(s):  
D. D. Lund ◽  
G. A. Davey ◽  
A. R. Subieta ◽  
B. J. Pardini
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Nerve Stimulation ◽  
Vagal Stimulation ◽  
Acetylcholinesterase Inhibition ◽  
Baroreflex Control ◽  
Recovery Mechanism ◽  
Vagal Innervation ◽  
Increased Sensitivity ◽  
Parasympathetic Control

Compensatory recovery by the intact vagal innervation after unilateral vagotomy was investigated by measuring parasympathetic-mediated control of heart rate in beta-adrenergic-blocked rabbits. Direct contralateral vagal nerve stimulation produced greater bradycardia in anesthetized rabbits with chronic vagotomy compared with acutely vagotomized controls. Vagal stimulation during acetylcholinesterase inhibition by physostigmine and direct neuroeffector stimulation by methacholine indicated that a change in metabolism of the neurotransmitter or an increased sensitivity of the tissue to acetylcholine were not responsible for augmentation of vagal responses. Baroreflex control of heart rate in response to an increase in arterial pressure was also tested in urethan-anesthetized rabbits. There was a significant reduction in the prolongation of the R-R interval during baroreflex activation acutely after midcervical vagotomy. These values were subsequently above control levels in rabbits 28 days after vagotomy. In conscious rabbits, the decrease in baroreflex control of heart rate progressively recovered to control levels within 6 days. These results suggest that the recovery mechanism after unilateral vagotomy may be related to peripheral and central compensatory changes in the intact contralateral vagus nerve.

Effect of hypoxic hypoxia on systemic vasculature

1984 ◽  
Vol 56 (5) ◽  
pp. 1403-1410 ◽  
Author(s):  
J. Malo ◽  
H. Goldberg ◽  
R. Graham ◽  
H. Unruh ◽  
C. Skoog
Keyword(s):  
Arterial Pressure ◽  
Inferior Vena ◽  
Superior Vena ◽  
Venous Pressure ◽  
Vena Cava ◽  
Venous Drainage ◽  
Hypoxic Hypoxia ◽  
Venous Compliance ◽  
Flow Curves ◽  
Pressure Flow

Effects of hypoxic hypoxia (HH) on cardiac output (CO), CO distribution, arterial and venous pressure-flow curves, vascular compliance, vascular time constant (tau), and resistance to venous return (RVR) were evaluated on six dogs. The vascular bed was isolated into four compartments depending on venous drainage: superior vena cava (SVC), splanchnic, renal and adrenal, and the remainder of the inferior vena cava (IVC). Low arterial O2 content and PO2 produced a threefold increase in CO at the same mean arterial pressure and a significant redistribution of CO to the SVC. Arterial pressure-flow curves decreased their slope (i.e., flow resistance) by a factor of two in the IVC and renal beds and by a factor of three in the splanchnic and SVC beds. Venous pressure-flow curves for the animal also decreased their slope significantly. HH causes a twofold increase in venous compliance and in mean venous pressure; tau did not change, but RVR halved. Seventy percent of the CO increase is explained by the increase in mean venous pressure and 30% by the reduction in RVR.

scholarly journals Identifying the role of group III/IV muscle afferents in the carotid baroreflex control of mean arterial pressure and heart rate during exercise

2018 ◽  
Vol 596 (8) ◽  
pp. 1373-1384 ◽  
Author(s):  
Thomas J. Hureau ◽  
Joshua C. Weavil ◽  
Taylor S. Thurston ◽  
Ryan M. Broxterman ◽  
Ashley D. Nelson ◽  
...  
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Muscle Afferents ◽  
Baroreflex Control ◽  
Group Iii ◽  
Carotid Baroreflex

Thyroid status influences baroreflex function and autonomic contributions to arterial pressure and heart rate

2001 ◽  
Vol 280 (5) ◽  
pp. H2061-H2068 ◽  
Author(s):  
C. Michael Foley ◽  
Richard M. McAllister ◽  
Eileen M. Hasser
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Logistic Function ◽  
Arterial Baroreflex ◽  
Thyroid Status ◽  
Baroreflex Control ◽  
Baroreflex Function ◽  
Resting Blood Pressure ◽  
Sympathetic Influence

The effect of thyroid status on arterial baroreflex function and autonomic contributions to resting blood pressure and heart rate (HR) were evaluated in conscious rats. Rats were rendered hyperthyroid (Hyper) or hypothyroid (Hypo) with triiodothyronine and propylthiouracil treatments, respectively. Euthyroid (Eut), Hyper, and Hypo rats were chronically instrumented to measure mean arterial pressure (MAP), HR, and lumbar sympathetic nerve activity (LSNA). Baroreflex function was evaluated with the use of a logistic function that relates LSNA or HR to MAP during infusion of phenylephrine and sodium nitroprusside. Contributions of the autonomic nervous system to resting MAP and HR were assessed by blocking autonomic outflow with trimethaphan. In Hypo rats, the arterial baroreflex curve for both LSNA and HR was shifted downward. Hypo animals exhibited blunted sympathoexcitatory and tachycardic responses to decreases in MAP. Furthermore, the data suggest that in Hypo rats, the sympathetic influence on HR was predominant and the autonomic contribution to resting MAP was greater than in Eut rats. In Hyper rats, arterial baroreflex function generally was similar to that in Eut rats. The autonomic contribution to resting MAP was not different between Hyper and Eut rats, but predominant parasympathetic influence on HR was exhibited in Hyper rats. The results demonstrate baroreflex control of LSNA and HR is attenuated in Hypo but not Hyper rats. Thyroid status alters the balance of sympathetic to parasympathetic tone in the heart, and the Hypo state increases the autonomic contributions to resting blood pressure.

scholarly journals Sex differences in blood pressure responsiveness to spontaneous K-complexes during stage II sleep

2020 ◽  
Author(s):  
Ian Mark Greenlund ◽  
Carl A. Smoot ◽  
Jason R. Carter
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Cardiac Cycle ◽  
Pressor Response ◽  
Systolic Arterial Pressure ◽  
Stage Ii ◽  
Men And Women ◽  
Blood Pressures ◽  
Blood Pressure Responses

K-complexes are a key marker of non-rapid eye movement sleep (NREM), specifically during stages II sleep. Recent evidence suggests the heart rate responses to a K-complexes may differ between men and women. The purpose of this study was to compare beat-to-beat blood pressure responses to K-complexes in men and women. We hypothesized that the pressor response following a spontaneous K-complex would be augmented in men compared to women. Ten men (Age: 23 ± 2 years, BMI: 28 ± 4 kg/m2) and ten women (Age: 23 ± 5 years, BMI: 25 ± 4 kg/m2) were equipped with overnight finger plethysmography and standard 10-lead polysomnography. Hemodynamic responses to a spontaneous K-complex during stable stage II sleep were quantified for 10 consecutive cardiac cycles, and measurements included systolic arterial pressure (SAP), diastolic arterial pressure (DAP), and heart rate. K-complex elicited greater pressor responses in men when blood pressures were expressed as SAP (cardiac cycle × sex: p = 0.007) and DAP (cardiac cycle × sex: p = 0.004). Heart rate trended to be different between men and women (cardiac cycle × sex: p = 0.078). These findings suggest a divergent pressor response between men and women following a spontaneous K-complex during normal stage II sleep. These findings could contribute to sex-specific differences in cardiovascular risk that exist between men and women.

Prostaglandin D2 inhibits hypoxic pulmonary vasoconstriction in neonatal lambs

1983 ◽  
Vol 54 (6) ◽  
pp. 1585-1589 ◽  
Author(s):  
J. B. Philips ◽  
R. K. Lyrene ◽  
M. McDevitt ◽  
W. Perlis ◽  
C. Satterwhite ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Inferior Vena ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Vena Cava ◽  
Systemic Arterial Pressure ◽  
Prostaglandin D2 ◽  
Pulmonary Vasoconstriction ◽  
Neonatal Lambs

Intrapulmonary injections of prostaglandin D2 (PGD2) reduce pulmonary arterial pressure and resistance in fetal and hypoxic neonatal lambs without affecting systemic arterial pressure. This apparently specific pulmonary effect of PGD2 could be explained by inactivation of the agent during passage through the pulmonary capillary bed. We therefore studied the effects of both pulmonary and systemic infusions of PGD2 on the acute vascular response to a 1-min episode of hypoxia in newborn lambs. Since PGD2 has been reported to be a pulmonary vasoconstrictor in normoxic lambs, we also evaluated its effects during normoxemia. Pulmonary vascular pressures were not affected by either 1- or 10-micrograms . kg-1 . min-1 infusions into the left atrium or inferior vena cava during normoxia. Infusion of 1 microgram . kg-1 . min-1 PGD2 into the inferior vena cava decreased pulmonary vascular resistance and increased systemic arterial pressure. These two parameters were unchanged with the other three infusion regimens. Mean pulmonary vascular resistance rose 83% with hypoxia and no PGD2. PGD2 prevented any change in pulmonary vascular resistance with hypoxia, while systemic arterial pressure increased (1-microgram . kg-1 . min-1 doses) or was unchanged. Thus PGD2 specifically prevents hypoxic pulmonary vasoconstriction while maintaining systemic pressures, regardless of infusion site. PGD2 may be indicated in treatment of persistent pulmonary hypertension of the newborn and other pulmonary hypertensive disorders.

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