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PubMed1993

Characterization of the neonatal heart rate baroreflex during and after ECMO.

Prolonged continuous blood pressure (BP) and heart rate (HR) recordings from neonates of 35 to 42 weeks gestation were studied during and after ECMO. Data segments with significant deviation of BP were extracted for further analysis. The simultaneous changes in BP and HR were compared and the slope of the regression determined baroreflex sensitivity (BRS). Of 464 BP deviations, 98% produced curves with a negative slope consistent with the presence of a baroreflex. The average BRS was -1.0 +/- 0.8 bpm/mmHg (mean +/- S.D.) and curves were steeper during rising BP than falling BP (-1.1 +/- 0.9 beats/min per mmHg versus -0.9 +/- 0.6, P = 0.001). The baroreflex was more sensitive during ECMO than after ECMO to both rising BP (-1.0 +/- 0.5 beats/min per mmHg versus -0.7 +/- 0.5, P = 0.004) and falling BP (-1.0 +/- 0.6 beats/min/mmHg versus -0.7 +/- 0.5, P = 0.04). HR response curves obtained during different BP fluctuations on the same recording had varying threshold, consistent with acute resetting. One infant demonstrated chronic baroreceptor resetting over 3 days to a rise in resting BP. The near-term, critically ill neonate has an active baroreflex which is capable of resetting. ECMO was associated with accentuation of the baroreflex response.

Blood Pressure↗
PubMed1980

Baroreflex sensitivity changes during the development of Goldblatt two-kidney one-clip hypertension in rats.

1. The time course of changes in baroreceptor reflex sensitivity during the development of renovascular hypertension was studied in male Wistar rats in which the left renal arteries were constricted by silver wire clips of 0.18 mm internal diameter. 2. Groups of animals were studied at 3, 7, 14 and 25 days after induction of renovascular hypertension. Rats of comparable ages were included as controls. There was a significant decrease in mean baroreflex sensitivity from 0.950 +/- 0.157 ms/mmHg (n = 8) in the normal control group to 0.537 +/- 0.105 ms/mmHg (n = 8) in the 3 day hypertensive group (P < 0.05). Baroreflex sensitivity in the 3 day hypertensive rats was independent of the level of arterial pressure achieved in individual animals. 3. These changes in baroreflex sensitivity at 3 days precede the development of left ventricular hypertrophy and, as previously shown in this model, also precede structural vascular adaptation and resetting of the carotid sinus baroreceptor threshold. 4. A further loss of baroreflex sensitivity, which may be structurally based, occurred later. Baroreflex sensitivity in the 14 day hypertensive rats fell to 0.182 +/- 0.039 ms/mmHg (n = 8) compared with the 3 day hypertensive rats (P < 0.01).

Animals↗
PubMed1981

Daily profile of baroreflex sensitivity and the variability of blood pressure in essential hypertensive patients.

1. We have monitored intra-arterial pressure continuously throughout the day and analysed every beat by computer. 2. Baroreflex sensitivity (ms/mmHg) was measured four times a day (07.00, 12.00, 17.00 and 20.00 hours) in seven patients and three times a day (07.00, 12.00 and 17.00 hours) in 23 patients. The diurnal variation of baroreflex sensitivity in individual patients was 0--5.3 ms/mmHg and was not consistent. Mean baroreflex sensitivity was reduced in hypertensive patients compared with normotensive subjects. 3. A negative correlation was seen between baroreflex sensitivity and the variability of systemic blood pressure. 4. Baroreflex sensitivity was well correlated with the variability of heart rate.

Adult↗
PubMed1982

The autonomic nervous tone abnormalities in the genesis of the impaired baroreflex responsiveness in borderline hypertensive subjects.

1. The effects of intravenous administration of neostigmine and propranolol, individually or in combination, on baroreflex responsiveness have been evaluated in 18 borderline hypertensive subjects and in 14 age-matched control subjects. 2. Baroreceptor sensitivity was tested by evaluating both heart rate response to phenylephrine-induced increase in arterial pressure, and heart rate and blood pressure changes induced by increasing neck-tissue pressure by means of a neck-chamber. 3. In borderline hypertensive subjects a reduced baroreflex responsiveness was demonstrated with both stimuli as compared with normal subjects. Neostigmine administration improved consistently both reflex responses. Similarly, after propranolol treatment, borderline hypertensive subjects showed a significant enhancement of the baroreflex sensitivity. Finally, the combined administration of neostigmine and propranolol restored the baroreflex responses. In fact, both the mean slopes of the regression lines between blood pressure and R-R interval after phenylephrine and the increase in mean arterial pressure and heart rate induced by the reduction in carotid transmural pressure in borderline hypertensive subjects were similar to those observed in normals. 4. These findings indicate that in borderline hypertensive subjects the impairment of baroreflex responsiveness is mainly due to abnormalities of autonomic regulation.

Adult↗
PubMed1992

Atrial natriuretic peptide and the baroreflex control of circulation.

An emerging role for atrial natriuretic peptide (ANP) as a modulator of baroreflex function is suggested by a number of experimental observations. In several animal species and in humans, ANP appears to reset the baroreflex control of heart rate in a way that favors bradycardia and opposes cardioacceleration. In addition, ANP interferes with the reflexes originating from cardiopulmonary receptors in the control of vascular tone. The modulation of baroreflexes by ANP seems to be related, at least in part, to the interaction of the atrial peptide with the effects of angiotensin II. This influence of ANP on the baroreflex control of circulation may be important in short-term cardiovascular adaptations, and may have particular relevance to conditions characterized by volume overload and impaired baroreflex function, such as certain forms of hypertension and congestive heart failure.

Animals↗
PubMed1980

Effect of coronary occlusion on arterial baroreflex control of heart rate.

To determine whether the baroreflex control of heart rate is altered during acute myocardial ischaemia, the baroreflex slope was measured at the control state, during coronary occlusion, and at the recovery phase in nine conscious dogs. The baroreflex slope was obtained by relating the R-R interval to the preceding systolic pressure during phenylephrine-induced transient hypertension. The baroreflex slope was reduced during coronary occlusion (18.8 +/- 3.8 ms.kPa-1, mean +/- SE) compared with that at the control state (41.4 +/- 6.0 ms.kPa-1). This reduction in the baroreflex slope during coronary occlusion was also present after propranolol, which suggests that this reduction of the slope during myocardial ischaemia is not due to a simultaneous increase in beta-adrenergic activity. These results suggest that the reflex originating from the cardiac receptors may modulate heart rate response to arterial baroreceptor stimulation.

Animals↗
PubMed1984

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.

Aged↗
PubMed1983

The arterial baroreflex and the cardiopulmonary reflex in borderline hypertension.

An elevation of the cardiopulmonary baroreflex control of the forearm vascular resistances due to an impairment of the arterial baroreflex has been postulated in borderline hypertension. The purpose of the study is to verify this hypothesis. The arterial baroreflex sensitivity, measured by the phenylephrine method is similar in borderline hypertensive and normotensive subjects of the same age. The forearm and the splanchnic vascular resistances are studied in borderline hypertension and normotension during leg negative body pressure at -40 and -70 mmHg. Baseline forearm resistances are higher in borderline hypertension. The increase of forearm resistance is similar in borderline hypertension and normotension when variations are expressed in percentage of the basal values. The elevation of plasma norepinephrine is similar in the two groups. The tachycardia and the elevation of splanchnic resistances are similar in borderline hypertensive and normotensive subjects. We conclude that: The arterial baroreflex is acting normally in borderline hypertension. The cardiopulmonary baroreflex control of the forearm vascular resistances is normal in borderline hypertension. The elevation of the basal forearm vascular resistances is not due to a sympathetic hyperactivity.

Adult↗
PubMed2002

Mental stress response, arterial stiffness, and baroreflex sensitivity in healthy aging.

This study examined the relationship of pressor responses during mental stress to arterial stiffness and baroreflex sensitivity. Hemodynamic responses of 24 healthy individuals (51-86 years old) to two mental stress tasks (math and speech) were compared with common carotid artery mechanical stiffness and autonomic nervous system regulation of blood pressure as measured by using the modified Oxford technique. At the ages studied, no effect of age on stress task responsiveness, carotid stiffness, or baroreflex sensitivity was observed. Carotid stiffness and baroreflex sensitivity demonstrated a strong inverse relation. Change in heart rate during the speech task was correlated with arterial stiffness, and the increase in mean arterial pressure was associated with carotid stiffness and was inversely correlated to baroreflex sensitivity. These associations suggest that acute hemodynamic reactions to mental stress among healthy adults are determined, in part, by structural properties of arterial vessels and sensitivity of arterial baroreflex. These observations may provide a mechanistic link between the physiology of cardiovascular reactivity to stress and risk of cardiovascular events in middle-aged and older individuals.

Aged↗
PubMed2002

Sinusoidal neck suction for evaluation of baroreflex sensitivity during desflurane and sevoflurane anesthesia.

UNLABELLED: Sevoflurane and desflurane modulate autonomic nervous activity by different mechanisms. We tested the hypothesis that these anesthetics also exhibit different effects on short-term baroreflex regulation of arterial blood pressure. Forty ASA physical status I patients, aged 20 to 42 yr, were randomly assigned to receive either 1.0 minimum alveolar anesthetic concentration of sevoflurane or desflurane for the maintenance of anesthesia. Patients were studied during awake conditions and 20 min after the anesthesia induction using sinusoidal neck suction at 0.2 Hz (baroreflex response mediated mainly by vagal activity) and 0.1 Hz (baroreflex response mediated by vagal and sympathetic activity), whereas respiratory frequency was fixed at 0.25 Hz. RR interval and arterial blood pressure responses were evaluated by power spectral analysis and complex transfer function analysis. Sevoflurane and desflurane did not disturb the linear relationship between baroreceptor stimulation and effector response, expressed as squared coherence of signals, i.e., the equivalent of the correlation coefficient of power spectra. Sevoflurane and desflurane depressed the response of the heart rate to neck suction in a similar way without affecting the time delay between baroreceptor stimulation and vagal-mediated cardiac response. The gain of the transfer function between neck suction and oscillation in arterial blood pressure at 0.1 Hz decreased with sevoflurane and desflurane to comparable values. Both anesthetics increased the delay of systolic blood pressure response to baroreceptor stimulation from approximately 3.5 to 4.3 s. Baroreflex-mediated short-term control of arterial blood pressure is similar between desflurane and sevoflurane during steady-state conditions. IMPLICATIONS: Despite exhibiting different effects on autonomic activity, sevoflurane and desflurane depress the baroreflex-mediated short-term control of heart rate and blood pressure in a similar manner.

Adult↗
PubMed1977

Halothane depresses baroreflex control of heart rate in man.

Baroreflex control of heart rate was determined during three awake control situations and during two depths of halothane anesthesia in man. Baroreflex function was quantiated by calculating the pressor test slope from the R-R interval change on the ECG produced by a pharmacologically induced pressor response. During the three awake control situations the subjects breathed room air or 100 per cent O2 spontaneously or 100 per cent O2 with ventilation controlled. Mean (+/- SD) slopes obtained were 15.1 +/- 4.5, 15.6 +/- 6.8 and 18.4 +/- 9.9, respectively. No significant difference in baroreflex function slope was observed. During light halothane anesthesia (0.7 per cent endtidal) baroreflex function was significantly depressed (mean slope = 2.5 +/- 1.5), and it was abolished at 1.1 per cent end-tidal halothane (mean slope = 0.03 +/- 0.04). It is concluded that halothane anesthesia produces depression of baroreflex control of heart rate in man.

Adult↗
PubMed1989

Limited baroreflex control of heart rate in young stroke-prone spontaneously hypertensive rats.

Controversy regarding possible differences of baroreflex gain in spontaneously hypertensive rats (SHR) and their relationship to the rise in blood pressure may be due in part to variations in the methods used to assess baroreflex function. In this study, we have compared the baroreflex control of heart rate in normotensive (Wistar-Kyoto, WKY) and stroke-prone spontaneously hypertensive (SHRSP) rats at 1 and at 7 months of age. Mean arterial pressure and heart rate were monitored in conscious rats following implantation of arterial and venous catheters. Phenylephrine and nitroprusside were given intravenously and the peak responses of mean arterial pressure and heart rate were recorded. In the young rats, these recordings were repeated under anaesthesia. Individual slopes for responses to phenylephrine or nitroprusside were obtained by linear regression. A single relationship covering both sets of responses was also obtained by fitting the data to a sigmoidal curve. The latter approach enabled the baroreflex to be represented as a single function which has a single determinant of gain, operates within defined limits and can be readily related to resting mean arterial pressure and heart rate. This approach demonstrated that: (1) in adult SHRSP, the baroreflex had reset to operate at higher resting levels of mean arterial pressure; (2) the range of heart rate control was smaller in both young and adult SHRSP compared with WKY; (3) average gain was slightly, but not significantly lower in adult SHRSP; (4) anaesthesia reduced heart rate range and average gain in both strains of rat.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1991

Reduced baroreflex changes in muscle sympathetic nerve activity during blood pressure elevation in essential hypertension.

To determine whether the baroreflex control of sympathetic nerve activity is altered in patients with essential hypertension, muscle sympathetic nerve activity (MSNA) was recorded microneurographically from the tibial nerves of 23 normotensive subjects and 23 patients with essential hypertension. When phenylephrine (2 micrograms/kg) was injected intravenously, although the pressor response of mean arterial blood pressure (MAP) was significantly enhanced in the hypertensives as compared with the normotensives, the reflex decrease in MSNA was significantly smaller in the hypertensives. Furthermore, the baroreflex slope for MSNA, used as an index of baroreflex sensitivity and calculated by relating the change in MSNA to the change in MAP, was significantly less in the hypertensives. Following the injection of nitroglycerin (2 micrograms/kg), there were no significant differences between the normotensives and hypertensives in the depressor response, the reflex increase in MSNA or the baroreflex slope for MSNA. These observations suggest that the baroreflex change in sympathetic nerve activity is reduced during phenylephrine-induced blood pressure elevation but not during nitroglycerin-induced hypotension in the hypertensives, and that the blunted response of sympathetic nerve activity occurring during hypertension in these hypertensive patients may underlie the maintenance of high blood pressure in essential hypertension.

Adult↗
PubMed1992

Differential effects of captopril and nicardipine on baroreflex control of sympathetic nerve activity and heart rate in renal hypertension.

OBJECTIVE: To test the hypothesis that an angiotensin I converting enzyme inhibitor and a calcium channel blocker have different effects on the arterial baroreflex in renal hypertension. DESIGN AND METHODS: We examined the baroreflex control of renal sympathetic nerve activity and heart rate before and after blood pressure was reduced by a similar magnitude (11 +/- 1 mmHg) with intravenous captopril or nicardipine in two-kidney, one clip hypertensive (mean arterial pressure 92 +/- 2 mmHg, n = 12) and normotensive rabbits (mean arterial pressure 75 +/- 1 mmHg, n = 9) in the conscious state. Data obtained during activation and deactivation of baroreceptors were analysed with logistic function curves, and the maximum slope of the curve was taken as the sensitivity of the baroreflex. RESULTS: The maximum slopes of the curves relating mean arterial pressure to renal sympathetic nerve activity and to the heart rate in hypertensive rabbits were significantly smaller than the maximum slopes in normotensive rabbits. In renal hypertensive rabbits, the maximum slope of the mean arterial pressure-renal sympathetic nerve activity curve was increased with captopril compared with that with vehicle. In contrast, the maximum slope of the mean arterial pressure-heart rate curve was increased with nicardipine compared with that with vehicle. CONCLUSIONS: Our data indicating that the baroreflex control of renal sympathetic nerve activity was improved by captopril and that baroreflex control of the heart rate was potentiated by nicardipine suggest that these classes of antihypertensive agents had differential effects in conscious hypertensive rabbits.

Angiotensin II↗
PubMed1988

Effect of acute and chronic indoramin administration on baroreflex function and tremor in humans.

Several mechanisms have been suggested for the absence of reflex tachycardia in response to the hypotensive effect of the selective alpha 1-adrenoceptor antagonist indoramin, including, in animals, membrane-stabilising activity, prolongation of repolarisation time, and reduction in baroreflex sensitivity. The present study investigated the effect of acute and chronic oral administration of indoramin (50 mg daily for 8 days) on baroreflex sensitivity in six healthy male volunteers. Baroreflex function was measured by determining the relationship between systolic blood pressure (SBP) and R-R interval following intravenous administration of phenylephrine. Indoramin shifted (p less than 0.05) the phenylephrine dose-response curve to the right on days 1 and 8 compared with placebo. Baroreflex sensitivity [R-R (ms)/SBP (mm Hg)] was reduced (p less than 0.05) by indoramin on day 1 compared with placebo (18.3 +/- 1.3 vs. 11.2 +/- 2.2 ms/mm Hg), and on day 8 compared with pretreatment values (18.3 +/- 2.8 vs. 10.8 +/- 1.8 ms/mm Hg). Acute but not chronic administration of indoramin caused (p less than 0.05) sedation; tremor tended to increase with chronic administration. It is suggested that depression of baroreflex sensitivity by indoramin may explain, in part, the lack of reflex tachycardia associated with its antihypertensive effect.

Adult↗
PubMed1990

An effect of trauma on human cardiovascular control: baroreflex suppression.

Survival from injury depends on the interaction between the patient's own homeostatic responses and treatment given. The function of the principal homeostatic reflex of the cardiovascular system, the arterial baroreflex, was studied in 22 healthy controls and in 21 moderately injured patients (ISS range, 9 to 17; median, 9) using suction stimulation of the carotid sinus baroreceptors. When compared to controls, marked baroreflex suppression was evident 3 hours after injury (p less than 0.05), at 3 days after injury (p less than 0.001), and even 15 days after injury (p less than 0.05, all Wilcoxon rank sum test). Partial recovery of baroreflex function occurred between 3 and 15 days after injury (p less than 0.005, all Wilcoxon signed rank test) and was complete by 5 months after injury. The suppression of baroreflex activity was accompanied by a "fixed" rise in heart rate and a rise in systolic blood pressure. This study has shown that moderate injury results in a profound and prolonged suppression of baroreflex function. Further advances in the resuscitation and critical care of the injured may need to take account of such derangements of cardiovascular physiology.

Adolescent↗
PubMedDate not supplied

Carotid baroreflex sensitivity at rest and during psychological stress in offspring of hypertensives and non-twin sibling pairs.

The baroreceptor reflexes of 38 young adult males were mechanically stimulated by negative external cervical pressure during a mental arithmetic task and pre-stress and post-stress relaxation periods. The subjects comprised 19 pairs of non-twin siblings. Baroreflex sensitivity was significantly less pronounced during arithmetic. Using non-invasive techniques, this finding replicates several others indicating a damping of the baroreceptor reflux during stress. More importantly, analyses of sibling similarities also revealed significant familiality of baroreflex sensitivity, independent of age, body mass, pressure applied and baseline heart rate. To examine the relationship between baroreflex sensitivity and parental history of hypertension, 21 young adult males with a parental history and 25 without participated in a second experiment. The two groups were not significantly different in resting baroreflex sensitivity. However, sensitivity was damped to a significantly greater degree during mental arithmetic in offspring of hypertensives, offering one possible explanation for their greater blood pressure reactivity to stress. These results suggest that familial influences may effect baroreflex sensitivity and, possibly as a result, blood pressure reactivity and risk for hypertension.

Adult↗
PubMed1986

Baroreflex sensitivity alteration following transient hemispheric ischaemia in rats: protective effect of alphamethyldopa and guanfacine.

The reflex tachycardia to arterial vasodilation was analysed in anaesthetized and ventilated Long Evans rats. Nicardipine was given by slow intravenous injection. The decrease in blood pressure was accompanied by a sympathetically mediated reflex tachycardia. The slope of the mean blood pressure-pulse period relationship was considered as an index of baroreflex sensitivity. Two injections of nicardipine were given during a single experiment. For studying the suprapontine control of the baroreflex arc, rats were subjected to transient (10 min) bilateral hemispheric ischaemia. These rats exhibited a blood pressure drop following recirculation and baroreflex sensitivity was impaired. Pretreatment with alpha-methyldopa, guanfacine and enalapril lowered mean blood pressure to a similar extent. In those rats pretreated with alpha-methyldopa and guanfacine transient hemispheric ischaemia did not alter baroreflex sensitivity while enalapril pretreated rats exhibited an impaired baroreflex. The protective effect of alpha-methyldopa and guanfacine against the cardiovascular consequence of hemispheric ischaemia may depend on reduced monoamine turnover resulting from central alpha-adrenoceptor stimulation.

Animals↗