Measure Of Baroreflex Sensitivity Research Articles

Normotensive Diabetic BB/W Rats Show Enhanced Reflex Tachycardia

Spontaneously diabetic BB/W rats were compared with age-matched regular Wistar and nondiabetic BB/W rats to determine whether the presence of diabetes would alter cardiovascular regulation appreciably. Systolic and mean blood pressures measured with the tail-cuff method from 12 to 26 wk of age tended to be slightly higher in diabetic than nondiabetic BB/W rats, but the differences were not significant. Mean pressures recorded from indwelling catheters in the same rats at 28 wk of age also did not differ significantly, thereby verifying that the diabetic rats were not hypertensive. To measure baroreflex sensitivity, heart-rate responses were elicited reflexly by elevating blood pressure with phenylephrine or lowering it with sodium nitroprusside. Although reflex bradycardia elicited with phenylephrine was the same, reflex tachycardia elicited with sodium nitroprusside was more pronounced in diabetic BB/W than other rats. Underlying autonomic mechanisms were then assessed by repeating the baroreflex tests after either cholinergic blockade with methylatropine or beta-adrenergic blockade with propranolol. Magnitude of reflex bradycardia after inhibition by either cholinergic or beta-adrenergic blockade still did not differ between rat groups but that of reflex tachycardia remained significantly stronger in diabetic BB/W than other rats. These results collectively show that, although diabetic BB/W rats remained normotensive, they had enhanced reflex tachycardia that persisted even after efferent autonomic blockade. The failure to develop higher pressures with time further indicates that without additional manipulation, these rats cannot be used experimentally to simulate the simultaneous presence of hypertension in diabetic patients.

Comparison of phenylephrine bolus and infusion methods in baroreflex measurements

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.

Comparison of baroreflex sensitivity and heart period variability after myocardial infarction

In animals, baroreflex sensitivity is inversely related to the likelihood of ventricular fibrillation during myocardial ischemia. After myocardial infarction in human patients, reduced baroreflex sensitivity is associated with increased mortality. A reduced standard deviation of normal RR intervals over a 24 h period is also associated with reduced survival after myocardial infarction. Therefore, 32 normotensive men who had survived their first myocardial infarction were studied to define the relation between baroreflex sensitivity assessed with phenylephrine injection and three Hotter electrocardiographic measures of tonic vagal activity: the percent of successive normal RR intervals >50 ms, the root mean square successive difference of normal RR intervals and the power in the high frequency energy of the normal RR interval power spectrum.Correlations among the Holter measures of heart period variability were ≥0.94, indicating that these measures are so strongly correlated that any one of them can be used to represent the others. Baroreflex sensitivity showed weaker correlations with the three Holter variables (0.57 to 0.63), indicating that the Holter measures did not accurately predict baroreflex sensitivity. Baroreflex sensitivity showed a stronger correlation with the three Hotter variables during the night than during the day. Baroreflex sensitivity and tonic vagal activity reflected by Holter variables were reduced more in patients with inferior myocardial infarction than in those with anterior infarction. The relative utility of baroreflex sensitivity and Holter measures of tonic vagal activity in predicting sudden cardiac death after myocardial infarction needs to be evaluated in a large prospective study.

Opiate receptor inhibition improves the blunted baroreflex function in conscious dogs with right-sided congestive heart failure.

The endogenous opiate system is activated in congestive heart failure. because endogenous opioids are known to depress the baroreflex function, we conducted studies to determine whether the increased endogenous opioids play a role in causing the reduced baroreflex function that occurs in heart failure. Right-sided congestive heart failure was produced in 16 dogs by tricuspid avulsion and progressive pulmonary artery constriction. Seven sham-operated dogs were included for comparison. Baroreflex function was measured in the conscious dogs after pretreatment with either normal saline or an opiate-receptor antagonist by bolus administration of phenylephrine. The slope of the regression line relating systolic blood pressure to cardiac cycle (R-R) interval was taken as an index of baroreflex sensitivity. Plasma beta-endorphin was elevated in the dogs with heart failure (15.3 +/- 2.5 pmol/l) compared with the sham-operated dogs (4.2 +/- 0.4 pmol/l, p less than 0.001). The dogs with heart failure also exhibited a reduced baroreflex sensitivity (3.84 +/- 0.19 msec/mm Hg) after saline pretreatment when compared with the sham-operated dogs (10.86 +/- 1.20 msec/mm Hg, p less than 0.001). Administration of naloxone hydrochloride increased the baroreflex sensitivity of dogs with heart failure to 5.16 +/- 0.26 msec/mm Hg (p less than 0.01) but produced no significant effects in sham-operated dogs (11.36 +/- 1.42 msec/mm Hg). To further study the site of action for the effect of naloxone, we measured baroreflex sensitivity in the dogs with heart failure after pretreatment with naloxonazine, a selective mu-receptor antagonist, with ICI 154,129, a selective delta-receptor antagonist, or with naloxone methobromide, a quaternary analogue of naloxone that does not penetrate the blood-brain barrier.(ABSTRACT TRUNCATED AT 250 WORDS)

Baroreflex sensitivity measured by the phenylephrine pressor test in patients with carotid sinus and sick sinus syndromes.

Baroreflex sensitivity was measured by the heart rate response to the transient rise in blood pressure induced by phenylephrine, in 11 patients with carotid sinus syndrome, 6 patients with sick sinus syndrome and nine age and blood pressure matched controls. Patients with carotid sinus syndrome were divided into those with a hypersensitive carotid sinus reflex manifest as sinus arrest (n = 9) and those with a reflex manifest as atrioventricular block (n = 2). The mean gain of the baroreflex sensitivity was significantly increased (p less than 0.001) in patients with carotid syndrome manifest as sinus arrest (12.7 +/- 5.1 ms . mmg-1) compared to that in patients with sick sinus syndrome (3.8 +/- 2.6 ms . mmHg-1) and controls (4.2 +/- 2.1 ms . mmHg-1). Patients with carotid sinus syndrome manifest as atrioventricular block did not have increased baroreflex sensitivity measured by their sinus node response (2.1 +/- 0.5 ms . mmHg-1). There was significant correlation (p less than 0.001) between the corrected carotid sinus inhibitory response to carotid sinus massage and the measurement of baroreflex sensitivity in the carotid sinus syndrome patients. Patients with carotid sinus syndrome manifest as reflex sinus arrest have an increased gain in baroreflex sensitivity for their age, which is not seen in patients with symptomatic sinoatrial disease. This study provides further evidence of a different mechanism of bradycardiac symptoms in patients with carotid sinus and sick sinus syndromes.

Involvement of the baroreceptor reflexes in the changes in blood pressure with sleep and mental arousal.

We have measured baroreflex sensitivity and blood pressure in 13 subjects during sleep and three stages of progressive mental arousal after waking. Baroreflex sensitivity was measured by correlating the increase in pulse interval with the increase in systolic pressure produced by an intravenous injection of 80 micrograms of phenylephrine. Blood pressure was measured directly from the brachial artery. During sleep, blood pressure fell and baroreflex sensitivity increased; with increasing mental arousal, blood pressure rose and baroreflex sensitivity decreased. These results suggest that baroreflex activity may be involved in the medium-term regulation of blood pressure during the day and night in addition to its recognized role in buffering acute changes in blood pressure.

The effect of phenylephrine upon arterial pressure, carotid sinus radius and baroreflex sensitivity in the conscious greyhound.

1. A method for recording carotid sinus diameter in conscious dogs has been developed, using an ultrasound transit time technique. We have used this method to measure the distensibility of the carotid sinus in resting animals, and we have investigated the effect of injecting the vasoactive drug phenylephrine on the mechanical behaviour of the sinus wall. 2. Baroreflex sensitivity was measured in the dogs by the usual method of relating the slowing of the heart to the transient pressure rise induced by the injections of phenylephrine. 3. We have shown that phenylephrine directly reduces the radius of the carotid sinus during the measurements of baroreflex sensitivity. At a dose of 2-4 micrograms/kg, phenylephrine has an enhancing effect on the baroreflex response, possibly resulting from a modification of baroreceptor output.

Plasma Noradrenaline as a Measure of Baroreflex Sensitivity in Hypertensive Man

1. Changes in plasma noradrenaline levels and heart rate were used as measures of baroreflex sensitivity in six hypertensive subjects given serial incremental doses of sodium nitroprusside (intravenously) to lower blood pressure. 2. The rises in both heart rate and plasma noradrenaline concentration were linearly related to the decrement in blood pressure and inversely related to the severity of the hypertension. 3. A positive correlation between rise in heart rate and rise in plasma noradrenaline was found for each subject. With increasing severity of hypertension, a greater increase in heart rate occurred for each increment in plasma noradrenaline concentration. 4. Baroreflex sensitivity can be assessed by relating changes in heart rate to change in arterial pressure; however, this method does not distinguish the relative contributions of the vagal and sympathetic components of the autonomic neural response or variations in the chronotropic response to sympathetic stimulation. 5. Changes in plasma noradrenaline levels in response to graded reductions in blood pressure may be a more appropriate measure of baroreflex sensitivity than the methods currently used in clinical investigation.

Autonomic dysfunction in Guillain-Barre syndrome.

The following tests of autonomic function were performed on seven patients with the Guillain-Barré syndrome and compared with controls: (1) measurement of heart rate and blood pressure in the supine and erect positions, (2) measurement of baroreflex sensitivity, (3) Valsalva's manoeuvre, (4) sweat test. In two patients the heart rates were fixed and greater than 100/min and in three there was postural hypotension. The baroflex sensitivity of four patients was abnormal and heart rate response to Valsalva's manoeuvre was impaired in two of the three patients who were able to perform the manoeuvre. Areas of anhidrosis were found in all seven patients. These abnormalities probably reflect pathological alterations of the sympathetic and parasympathetic components of the autonomic nervous system of patients with Guillain-Barré syndrome. The severity of autonomic involvement is not related to the degree of sensory and motor disturbance which is consistent with the patchy distribution of lesions throughout the peripheral and autonomic nervous systems.

Baroreceptor reflex sensitivity after acute blood volume expansion in anesthetized dogs.

Changes in heart rate resulting from mechanically induced changes in arterial blood pressure were used as a measure of baroreflex sensitivity. This sensitivity was shown to be decreased after volume expansion.

The Effect of Mental Arithmetic on Blood Pressure Variability and Baroreflex Sensitivity in Man

1. Baroreflex sensitivity was tested in three normal, three borderline and one hypertensive subject before and during mental arithmetic, the prolongation of pulse interval caused by a provoked rise in blood pressure being used as a measure of baroreflex sensitivity. 2. Baroreflex sensitivity was significantly decreased during mental arithmetic. 3. During mental arithmetic the arterial pressure fluctuated markedly. 4. These findings suggest that in man, as well as animals, the defence of alerting reaction depresses baroreflex control and thus contributes to the rise in blood pressure seen at this time.

Baroreflex sensitivity and responses to the Valsalva manoeuvre in subjects with diabetes mellitus.

Baroreflex sensitivity was measured in a group of diabetic patients from the slope of the regression of pulse interval on systolic arterial pressure, during elevation of pressure induced by phenylephrine. The response to Valsalva's manoeuvre was assessed in the same subjects. There was a good correlation between the two tests in the identification of patients with a parasympathetic autonomic disturbance, but measurements of baroreflex sensitivity were more readily quantifiable than were the responses to Valsalva's manoeuvre. Furthermore, baroreflex sensitivity could be measured in patients with sympathetic nervous dysfunction in whom vagal function could not be assessed by means of the Valsalva manoeuvre. Measurement of baroreflex sensitivity is likely to be suitable for longitudinal studies of the progress of diabetic autonomic neuropathy.

Dynamic effects of sinusoidal tilting on heart rate of healthy and paralyzed persons.

ArticleDynamic effects of sinusoidal tilting on heart rate of healthy and paralyzed persons.L L Hamilton, O Lindan, and J B ReswickL L Hamilton, O Lindan, and J B ReswickPublished Online:01 Sep 1969https://doi.org/10.1152/jappl.1969.27.3.378MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationCited ByReview of Perioperative Music Medicine: Mechanisms of Pain and Stress Reduction Around Surgery4 February 2022 | Frontiers in Medicine, Vol. 9Heart rate variability response to alcohol, placebo, and emotional picture cue challenges: Effects of 0.1-Hz stimulationPsychophysiology, Vol. 45, No. 5Characteristics of Resonance in Heart Rate Variability Stimulated by Biofeedback13 July 2006 | Applied Psychophysiology and Biofeedback, Vol. 31, No. 2Effects on baroreflex sensitivity measurements when different protocols are used to induce regular changes in beat-to-beat intervals and systolic pressure25 March 2004 | Physiological Measurement, Vol. 25, No. 2Frequency-Specific Amplification of Heart Rate Rhythms Using Oscillatory TiltPsychophysiology, Vol. 29, No. 1 More from this issue > Volume 27Issue 3September 1969Pages 378-84 https://doi.org/10.1152/jappl.1969.27.3.378PubMed5804137History Published online 1 September 1969 Published in print 1 September 1969 Metrics