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.

Baroreflex dysfunction in diabetes mellitus. I. Selective impairment of parasympathetic control of heart rate

1994 ◽  
Vol 266 (1) ◽  
pp. H235-H243 ◽  
Author(s):  
T. S. McDowell ◽  
M. W. Chapleau ◽  
G. Hajduczok ◽  
F. M. Abboud
Keyword(s):  
Diabetes Mellitus ◽  
Heart Rate ◽  
Blood Glucose ◽  
Arterial Pressure ◽  
Adrenergic Blockade ◽  
Baroreflex Control ◽  
Parasympathetic Control ◽  
Diabetic Rabbits ◽  
Selective Impairment ◽  
Increased Pressure

The purpose of this study was to determine the effect of diabetes mellitus on baroreflex control of heart rate. Diabetes (blood glucose = 378 +/- 21 mg/dl) was induced in rabbits by alloxan (n = 9). Alloxan-treated rabbits that remained normoglycemic (n = 9) and rabbits given saline instead of alloxan (n = 5) served as controls. Baroreflex control of heart rate was evaluated in conscious rabbits by measuring changes in heart rate during phenylephrine-induced increases and nitroglycerin-induced decreases in arterial pressure. In diabetic rabbits, the gain of the baroreflex-mediated bradycardia in response to increased pressure decreased significantly from -1.8 +/- 0.3 beats.min-1 x mmHg-1 before alloxan (n = 9) to -0.9 +/- 0.1 and -0.9 +/- 0.3 beats.min-1 x mmHg-1 after 12 and 24 wk of diabetes, respectively (n = 8; P < 0.05). There was no significant change in baroreflex gain in either alloxan-treated or saline-treated normoglycemic rabbits. Baroreflex-mediated bradycardia was not influenced significantly after beta-adrenergic blockade with propranolol (1 mg/kg) and was still impaired in diabetic vs. control rabbits after propranolol. The gain of the baroreflex-mediated tachycardia in response to decreased pressure was not altered in any of the three groups. Propranolol significantly decreased but did not abolish baroreflex-mediated tachycardia. Neither the vagal nor the sympathetic component of the tachycardia was altered significantly by diabetes.(ABSTRACT TRUNCATED AT 250 WORDS)

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

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.

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.

Impaired baroreflex control of vascular resistance in prehypertensive Dahl S rats

1983 ◽  
Vol 245 (2) ◽  
pp. H210-H217 ◽  
Author(s):  
F. J. Gordon ◽  
A. L. Mark
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Strain Difference ◽  
Sympathetic Innervation ◽  
Baroreflex Control ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Elevated Arterial Pressure

The purpose of this study was to examine baroreflex control of vascular resistance and heart rate in prehypertensive Dahl salt-sensitive (DS) and salt-resistant (DR) rats. Urethan-anesthetized normotensive DS rats demonstrated significantly impaired baroreflex control of both hindlimb vascular resistance and heart rate. This impairment was not secondary to elevated arterial pressure since blood pressure did not differ between DR and DS rats fed a low sodium diet. Vascular baroreflex responses were shown to depend on the integrity of efferent sympathetic innervation and to be mediated by the sinoaortic afferent arterial baroreceptors. No strain difference was observed for hindlimb vasodilation produced by papaverine or graded doses of nitroprusside, indicating that differences in resistance vessel vasodilator capacity or responsiveness could not account for differences in baroreflex responses. Since impaired baroreflex control was evident in DS rats prior to any elevation in arterial pressure, this abnormality may contribute to the DS rat's genetic propensity to develop hypertension.

Modulation of carotid sinus baroreceptor reflex by sciatic nerve stimulation

1975 ◽  
Vol 228 (5) ◽  
pp. 1535-1541 ◽  
Author(s):  
M Kumada ◽  
K Nogami ◽  
K Sagawa
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Sciatic Nerve ◽  
Arterial Pressure ◽  
Nerve Stimulation ◽  
Carotid Sinus ◽  
Peripheral Resistance ◽  
Baroreceptor Reflex ◽  
Equilibrium Pressure ◽  
Sciatic Nerve Stimulation

In anethetized, immobilized, and vagotomized cats we analyzed the effect of sciatic nerve stimulation (SNS) on the relationships between intrasinus pressure (ISP) and arterial pressure (AP) and between ISP and heart rate (HR). At each of seven ISP levels between 60 and 240 mmHg, AP and HR before and 20 s after the onset of SNS were plotted against ISP to obtain the ISP-AP and ISP-HR relationships before and during SNA. SNA caused increases in AP, HR, and total peripheral resistance (TPR) and a decrease in cardiac output (CO). SNS raised the equilibrium pressure (the value of AP at which AP equaled ISP), but it significantly (P smaller than 0.005) decreased the slope (or gain) of the ISP-AP relationship at ISP's between 90 and 150 mmHg. SNS also significantly (P smaller than 0.05) diminished the gain of ISP-HR relationship at ISP's between 120 and 210 mmHg. Modulation of the gain of ISP-AP relationship was ascribable to that of CO but not of TPR. We conclude that in vagotomized cats 1) SNS attenuates the sensitivity of AP and HR responses in the carotid sinus baroreceptor reflex, and 2) the inhibition of the reflex AP response was caused by modulation of the reflex CO response.

Augmented catecholamine uptake by the heart during hemorrhage in the conscious dog

1986 ◽  
Vol 250 (1) ◽  
pp. H76-H81 ◽  
Author(s):  
O. L. Woodman ◽  
J. Amano ◽  
T. H. Hintze ◽  
S. F. Vatner
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Coronary Blood Flow ◽  
Coronary Sinus ◽  
Nerve Stimulation ◽  
Left Ventricular ◽  
Sympathetic Nerve Stimulation ◽  
Net Release

Changes in arterial and coronary sinus concentrations of norepinephrine (NE) and epinephrine (E) in response to hemorrhage were examined in conscious dogs. Hemorrhage (45 +/- 3.2 ml/kg) decreased mean arterial pressure by 47 +/- 6%, left ventricular (LV) dP/dt by 38 +/- 6%, and mean left circumflex coronary blood flow by 47 +/- 6%, while heart rate increased by 44 +/- 13%. Increases in concentrations of arterial NE (5,050 +/- 1,080 from 190 +/- 20 pg/ml) and E (12,700 +/- 3,280 from 110 +/- 20 pg/ml) were far greater than increases in coronary sinus NE (1,700 +/- 780 from 270 +/- 50 pg/ml) and E (4,300 +/- 2,590 from 90 +/- 10 pg/ml). Net release of NE from the heart at rest was converted to a fractional extraction of 66 +/- 9% after hemorrhage. Fractional extraction of E increased from 16 +/- 6% at rest to 73 +/- 8% after hemorrhage. In cardiac-denervated dogs, hemorrhage (46 +/- 2.8 ml/kg) decreased mean arterial pressure by 39 +/- 15%, LV dP/dt by 36 +/- 10%, and mean left circumflex coronary blood flow by 36 +/- 13%, while heart rate increased by 24 +/- 10%. Hemorrhage increased arterial NE (1,740 +/- 150 from 210 +/- 30 pg/ml) and E (3,050 +/- 880 from 140 +/- 20 pg/ml) more than it increased coronary sinus NE (460 +/- 50 from 150 +/- 30 pg/ml) and E (660 +/- 160 from 90 +/- 20 pg/ml) but significantly less (P less than 0.05) than observed in intact dogs. These experiments indicate that hemorrhage, unlike exercise and sympathetic nerve stimulation, does not induce net overflow of NE from the heart.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Chronic baroreflex activation restores spontaneous baroreflex control and variability of heart rate in obesity-induced hypertension

2013 ◽  
Vol 305 (7) ◽  
pp. H1080-H1088 ◽  
Author(s):  
Radu Iliescu ◽  
Ionut Tudorancea ◽  
Eric D. Irwin ◽  
Thomas E. Lohmeier
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Arterial Pressure ◽  
Cardiac Arrhythmias ◽  
High Fat Diet ◽  
Renal Denervation ◽  
Gradual Increase ◽  
High Fat ◽  
Baroreflex Control ◽  
Cardiovascular Dynamic

The sensitivity of baroreflex control of heart rate is depressed in subjects with obesity hypertension, which increases the risk for cardiac arrhythmias. The mechanisms are not fully known, and there are no therapies to improve this dysfunction. To determine the cardiovascular dynamic effects of progressive increases in body weight leading to obesity and hypertension in dogs fed a high-fat diet, 24-h continuous recordings of spontaneous fluctuations in blood pressure and heart rate were analyzed in the time and frequency domains. Furthermore, we investigated whether autonomic mechanisms stimulated by chronic baroreflex activation and renal denervation—current therapies in patients with resistant hypertension, who are commonly obese—restore cardiovascular dynamic control. Increases in body weight to ∼150% of control led to a gradual increase in mean arterial pressure to 17 ± 3 mmHg above control (100 ± 2 mmHg) after 4 wk on the high-fat diet. In contrast to the gradual increase in arterial pressure, tachycardia, attenuated chronotropic baroreflex responses, and reduced heart rate variability were manifest within 1–4 days on high-fat intake, reaching 130 ± 4 beats per minute (bpm) (control = 86 ± 3 bpm) and ∼45% and <20%, respectively, of control levels. Subsequently, both baroreflex activation and renal denervation abolished the hypertension. However, only baroreflex activation effectively attenuated the tachycardia and restored cardiac baroreflex sensitivity and heart rate variability. These findings suggest that baroreflex activation therapy may reduce the risk factors for cardiac arrhythmias as well as lower arterial pressure.

scholarly journals Some Aspects of the Physiology and Anatomy of the Cardiovascular System of the Ferret, Mustela Putorius Furo

1979 ◽  
Vol 13 (3) ◽  
pp. 215-220 ◽  
Author(s):  
P. L. R. Andrews ◽  
A. J. Bower ◽  
O. Illman
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Vagal Stimulation ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Resting Heart Rate ◽  
Mustela Putorius ◽  
Arterial Blood ◽  
Great Vessels ◽  
Vagal Innervation

Summary The resting heart rate was monitored in SO urethane-anaesthetized (387 ± 54 beats/min) and 4 conscious (341 ± 39 beats/min) ferrets. The arterial blood pressure in the anaesthetized animals was 140/110 ± 35/31 mmHg. The circulatory responses to vagal stimulation, carotid artery occlusion and a variety of humoral agents were examined. The vagal innervation of the heart and of the distribution of the great vessels are described.

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