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PubMed2000

Effect of G-suit protection on carotid-cardiac baroreflex function.

INTRODUCTION: To test the hypothesis that G-suit inflation could increase cardiac chronotropic responses to baroreceptor stimulation and enhance baroreflex buffering of BP, the carotid-cardiac baroreflex response of 12 subjects was measured across two levels of lower body negative pressure (LBNP = 0 and 50 mm Hg) and two levels of G-suit inflation (0 and 50 mm Hg) in random order. METHODS: Carotid-cardiac baroreflex stimulation was delivered via a silastic neck pressure cuff and responsiveness quantified by determination of the maximum slope of the stimulus-response function between R-R intervals (ms) and their respective carotid distending pressures (mmHg). RESULTS: Mean +/- SE baseline control baroreflex responsiveness was 3.8+/-0.4 ms x mm Hg(-1). LBNP reduced the baroreflex response to 2.7+/-0.4 ms x mm Hg(-1), but G-suit inflation with LBNP restored the baroreflex response to 4.3+/-0.6 ms x mm Hg(-1). CONCLUSIONS: These results suggest that, in addition to increased venous return and elevated peripheral resistance, G-suit inflation may provide protection against the debilitating effects of blood distribution to the lower extremities during orthostatic challenges such as standing or high +Gz acceleration by increasing cardiovascular responsiveness to carotid baroreceptor stimulation.

Adult↗
PubMed1992

Myocardial infarction and baroreflex sensitivity. Clinical studies.

Based on solid experimental evidence the concept has emerged that analysis of autonomic reflexes, and specifically of baroreceptive reflexes, might contribute to the identification of high risk subgroups in the post myocardial infarction phase. Accordingly, we brought this concept to clinical fruition and have performed the first clinical study to investigate the potential prognostic value of baroreflex sensitivity. The present article reviews those clinical results which indicate an almost 15 times greater risk for cardiac mortality among the patients with depressed baroreflex sensitivity. Baroreflex sensitivity has also been correlated with heart rate variability and it was found that the degree of correlation is relatively weak and such that it is not possible to predict one measure from the other. Thus, these two autonomic markers are not redundant. Among the various possibilities to induce favorable alterations in the autonomic balance, our group has selected and analyzed exercise training and the chronic administration of beta-blocking agents. Exercise training, examined in a case-control study involving 70 patients, was found to increase baroreflex sensitivity by 30%. Beta-blockers were found to augment baroreflex sensitivity in 40% of the patients tested. As a logical evolution of these studies we have initiated a large prospective collaborative study destined to enroll 1200 post myocardial infarction patients and to assess the prognostic value of baroreflex sensitivity, of heart rate variability, and of traditional markers such as left ventricular ejection fraction and late potentials.

Clinical Trials as Topic↗
PubMed1992

Effects of acute exercise on attenuated vagal baroreflex function during bed rest.

We measured carotid baroreceptor-cardiac reflex responses in six healthy men, 24 h before and 24 h after a bout of leg exercise during 6 degrees head-down bed rest to determine if depressed vagal baroreflex function associated with exposure to microgravity environments could be reversed by a single exposure to acute intense exercise. Baroreflex responses were measured before bed rest and on day 7 of bed rest. An exercise bout consisting of dynamic and isometric actions of the quadriceps at graded speeds and resistances was performed on day 8 of bed rest and measurements of baroreflex response were repeated 24 h later. Vagally-mediated cardiac responses were provoked with ramped neck pressure-suction sequences comprising pressure elevations to +40 mm Hg, followed by serial, R-wave triggered 15 mm Hg reductions, to -65 mm Hg. Baroreceptor stimulus-cardiac response relationships were derived by plotting each R-R interval as a function of systolic pressure less the neck chamber pressure applied during the interval. Compared with pre-bed rest baseline measurements, 7 d of bed rest decreased the gain (maximum slope) of the baroreflex stimulus-response relationship by 16.8 +/- 3.4% (p < 0.05). On day 9 of bed rest, 24 h after exercise, the maximum slope of the baroreflex stimulus-response relationship was increased (p < 0.05) by 10.7 +/- 3.7% above pre-bed rest levels and 34.3 +/- 7.9% above bed rest day 7. Our data verify that vagally-mediated baroreflex function is depressed by exposure to simulated microgravity and demonstrate that this effect can be acutely reversed by exposure to a single bout of intense exercise.

Adult↗
PubMed1989

Comparison of arterial baroreflex function in humans anesthetized with enflurane or isoflurane.

To compare the depressive effects of isoflurane and enflurane on the arterial baroreflex function, we examined baroreflex control of heart rate during the entire course of clinical anesthesia. Isoflurane and enflurane were found to have similar depressive effects on the baroreflex control of heart rate when used in combination with N2O and O2. Suppression in the baroreflex sensitivity, defined by the slopes of regression line (change in msec of RR interval per mm Hg increase or decrease in systolic blood pressure) was from 7.1 +/- 3.9 to 1.8 +/- 0.7 msec/mm Hg in patients given isoflurane and from 7.8 +/- 4.3 to 3.0 +/- 1.9 msec/mm Hg in those given enflurane when evaluated by a pressor test (bolus IV phenylephrine). The slope of the depressor test (bolus IV nitroglycerin) also decreased from 4.7 +/- 2.8 to 1.9 +/- 1.5 msec/mm Hg with isoflurane and from 5.6 +/- 3.2 to 2.3 +/- 1.2 msec/mm Hg with enflurane. During surgery in which anesthetic concentration invariably needed to be increased, the suppression of the baroreflex sensitivity remained unchanged in both groups of patients. During recovery, the arterial baroreflex function in patients given isoflurane recovered more rapidly than that in patients given enflurane. This difference may be related to a more minor degree of suppression of isoflurane on the autonomic nervous system compared to enflurane.

Adult↗
PubMed1986

Effects of diazepam and midazolam on baroreflex control of heart rate and on sympathetic activity in humans.

The effects of induction of anesthesia with diazepam and midazolam on baroreflex control of heart rate and on plasma levels of catecholamines were investigated in this study. Group 1 subjects (n = 10) received diazepam, 0.4 mg/kg. Group 2 subjects (n = 10) received midazolam, 0.3 mg/kg. Baroreflex function was assessed using a pressor test (phenylephrine). In addition, samples for subsequent determination of plasma norepinephrine and epinephrine levels and plasma diazepam or midazolam concentrations were collected before and 5, 10, and 15 min after intravenous drug administration. The pressor baroreflex slope declined significantly after diazepam or midazolam administration with the maximal changes (-45 and -43%, respectively) observed when plasma diazepam or midazolam concentrations were the highest. Norepinephrine plasma concentrations decreased at each measurement with both drugs. In contrast, epinephrine concentration decreased only after midazolam. The authors conclude that diazepam or midazolam used for induction of anesthesia results in a transient depression of baroreflex function and a sustained decrease of sympathetic tone. This study also indicates that the depression of arterial baroreflex heart rate responses under diazepam or midazolam anesthesia are less pronounced than the depression of baroreflex responses reported by other investigators with potent inhalational anesthetics. However, this disruptive effect of diazepam and midazolam on sympathetic control of circulation might induce a limited ability to compensate for hemodynamic alterations related to hypovolemia.

Adult↗
PubMed1987

Abnormal cardiopulmonary baroreflexes in normotensive young subjects with a family history of essential hypertension.

Cardiopulmonary baroreflex control of forearm vascular resistance (FVR) and arterial baroreflex control of heart rate were compared between 12 normotensive subjects with hypertensive relatives (group A, 19.4 +/- 0.2 years) and 12 normotensive subjects with no family history of hypertension (group B, 19.5 +/- 0.3 years). Cardiopulmonary baroreflexes were evaluated using lower body negative pressure (LBNP) at -20 mmHg, and arterial baroreflexes were measured by Oxford phenylephrine method. Resting arterial pressure, central venous pressure, heart rate, cardiac index, total peripheral resistance, and FVR were not different between the two groups. Arterial baroreflex slope (BS) and reflex increases in FVR during LBNP were significantly lower in group A than in group B (11.4 +/- 0.9 vs. 17.1 +/- 1.1 ms/mmHg, 37.7 +/- 8.1% vs. 86.5 +/- 18.7%, respectively). There was significant correlation between %FVR and BS (r = 0.59; p less than 0.01). These results suggest that both cardiopulmonary and arterial baroreflexes are impaired in normotensive young subjects with a family history of hypertension.

Adolescent↗
PubMed2000

Stability of the noninvasive baroreflex sensitivity assessment using cross-spectral analysis of heart rate and arterial blood pressure variabilities.

BACKGROUND: Depressed baroreflex sensitivity (BRS), usually estimated using the invasive phenylephrine method or the nitroprusside test, is significantly and independently associated with an increased risk of malignant ventricular arrhythmias and sudden cardiac death in patients surviving acute myocardial infarction. Several investigators have compared the standard phenylephrine test and different noninvasive methods. HYPOTHESIS: This study evaluated the influence of different body positions with different breathing regimes on cross-spectral baroreflex indices (coherence between the spectral densities of blood pressure and cardiac cycle variabilities) in both low- and high-frequency bands. METHODS: The data were obtained in 103 patients (73 males, aged 53 +/- 12 years) with coronary artery disease and/or hypertension. Simultaneous electrocardiographic and noninvasive blood pressure recordings were obtained in each subject in both supine and sitting positions during both spontaneous and slow and fast controlled respiration (0.1 and 0.33 Hz). RESULTS: The results show a significant bias and disagreement between noninvasive baroreflex sensitivity (BRS) indices. The mean values of the baroreflex in low frequency ranged from 5.0 +/- 5.3 to 10.1 +/- 7.9 ms/mmHg, while in high frequency, the mean values ranged from 6.6 +/- 6.1 to 10.1 +/- 7.9 ms/mmHg. The limits of agreement ranged from +/-1.7 to +/-4.1 ms/mmHg with bias from -1.0 to +0.7 ms/mmHg. CONCLUSION: A comprehensive comparison of different methods shows that BRS estimated in low-frequency band in sitting position during spontaneous respiration is the most representative part of the global baroreflex gain.

Adult↗
PubMedDate not supplied

Parabrachial nucleus induces suppression of baroreflex bradycardia by the release of glutamate in the rostral ventrolateral medulla of the rat.

The involvement of glutamatergic neurotransmission in the rostral ventrolateral medulla (RVLM) in the suppression of baroreflex bradycardia by the parabrachial nucleus (PBN) was investigated. Repeated electrical activation of the PBN increased the concentration of glutamate in the dialysate collected from the RVLM. The same stimulation also suppressed baroreflex bradycardia in response to transient hypertension evoked by phenylephrine (5 microg/kg, intravenously). Microinfusion of L-glutamate (10, 50 or 100 microM) via the microdialysis probe into the RVLM dose-dependently elicited a significant inhibition of baroreflex bradycardia that paralleled the concentration and time course of the PBN-elicited elevation in extracellular glutamate in the RVLM. The suppression of baroreflex bradycardia elicited by microinjection of L-glutamate (1 nmol) into the RVLM was appreciably reversed by coinjection of the NMDA receptor antagonist, dizocilpine (500 pmol), or the non-NMDA receptor antagonist, 6-cyano-7-nitroquinoxaline-2, 3-dione (50 pmol). These results suggest that an increase in the extracellular concentration of glutamate and activation of both NMDA and non-NMDA receptors in the RVLM may mediate the suppression of baroreflex bradycardia by activation of the PBN.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1999

Baroreflex sensitivity is depressed in microalbuminuric Type I diabetic patients at rest and during sympathetic manoeuvres.

AIMS/HYPOTHESIS: To evaluate baroreflex sensitivity (BRS) in microalbuminuric and normoalbuminuric Type I (insulin-dependent) diabetic patients without autonomic neuropathy and in healthy control subjects. METHODS: Microalbuminuric Type I diabetic patients (n = 15) were matched for age, sex, body mass index (BMI) and smoking habits with 15 normoalbuminuric patients and with 15 healthy control subjects. All subjects had a blood pressure less than 160/95 mmHg, a BMI less than 30 kg/m(2) and normal autonomic function on standard tests. Blood pressure and heart rate were measured non-invasively (Finapres) at rest and during sympathetic activation (handgrip, mental stress, standing). The baroreflex sensitivity was defined as the mean gain between blood pressure variability and heart rate variability in the 0.07-0.15 Hz frequency band. RESULTS: Resting baroreflex sensitivity was decreased in the microalbuminuric patients (3.5 +/- 0.4 ms/mmHg) compared with the normoalbuminuric patients and the healthy subjects (7.6 +/- 1.6 and 9.5 +/- 1.1 ms/mmHg, respectively, p < 0.001). The sympathetic tests reduced baroreflex sensitivity similarly in the groups without changing the between group differences. CONCLUSION/INTERPRETATION: Baroreflex sensitivity is reduced in Type I diabetic patients with microalbuminuria but without autonomic neuropathy. A prospective study should indicate whether this early abnormality in cardiovascular reflex function is a risk factor of cardiovascular mortality in these patients. [Diabetologia (1999) 42: 1345-1349]

Albuminuria↗
PubMed2002

[Recurrent hypertensive crises associated with severe orthostatic hypotension due to baroreflex failure syndrome].

The baroreflex mechanism is a central part of the regulation of the cardiovascular system, particularly in the control of vagal and sympathetic outflow to the heart and the peripheral circulation. Failure of the baroreflex is a rare cause of secondary hypertension. It is characterized by drastic changes in sympathetic activation and blood pressure following complete denervation of the baroreflex. Here, we report a case of baroreflex failure following bilateral carotid artery surgery and radiation. Moreover, postoperative orthostatic hypotension with recurrent syncope suggests a rare subform, the selective baroreflex failure, where efferent parasympathetic activity is preserved. Both high blood pressure and orthostatically induced syncope improved substantially after treatment with clonidine.

Baroreflex↗
PubMed2004

Long-term effects of unilateral carotid endarterectomy on arterial baroreflex function.

BACKGROUND AND PURPOSE: Carotid endarterectomy (CE) may be complicated by the clinical syndrome of baroreflex failure. Alterations of baroreflex function may also account for the frequently observed blood pressure lability in the first hours following surgery. We investigated the long-term effects of unilateral CE on baroreflex control of function and blood pressure. METHODS: We investigated 14 patients after unilateral CE (13 m:1 f, 64.8 +/- 6.5 years), 9 patients with a surgically untreated uni-/bilateral carotid stenosis (CS, 7 m:2 f, 57.6 +/- 10.7 years) and 12 healthy controls (HC, 11 m:1 f, 60.9 +/- 7.9 years) by means of Valsalva maneuver, active standing, forced breathing, cold face test, cold pressor test and mental arithmetic. Ambulatory blood pressure level and variability were determined from 24-hour Spacelabs and 5-hour beat-to-beat Portapres recordings. RESULTS: Baroreflex sensitivity (derived from phase IV Valsalva maneuver) was significantly lower in CE (1.53 +/- 0.83 ms/mmHg) than in CS (4.39 +/- 2.27, p = 0.002) and HC (5.34 +/- 3.78, p = 0.003). CE patients exhibited a decreased reflex control of heart rate in response to Valsalva's maneuver and active standing without orthostatic hypotension. Office blood pressure levels before and after endarterectomy were similar, as were ambulatory blood pressure levels in the three groups. Ambulatory blood pressure variability was higher in CE and CS than in HC, but not different between CE and CS. CONCLUSIONS: Unilateral CE causes a long-term impairment of baroreflex function, resulting in an attenuated reflex control of heart rate, but no hypertension or blood pressure lability.

Adult↗
PubMed2006

The cold face test: a non-baroreflex mediated test of cardiac vagal function.

Application of cold to the face evokes potent bradycardia and a pressor response, similar to the diving reflex. However, the role of the baroreceptors in this response is unclear. Ten healthy controls and two patients with baroreflex impairment were recruited. A cold face test (CFT) was induced by the application of three cold packs (0.5 degrees C) to the face. Heart rate (ECG), blood pressure (Finapres) and skin temperature (forehead electrode) were recorded continuously. All data were analyzed using unpaired Students t-tests, and expressed as mean +/- SD. In all controls, CFT induced bradycardia. The mean onset latency was 5.6 +/- 4.6 s, and the maximal bradycardia was seen at 35.8 +/- 15.8 s. Systolic blood pressure increased in eight controls, with a mean onset latency of 18.8 +/- 16.6 s and a peak rise at 38.7 +/- 22.7 s. In the controls, bradycardia preceded the pressor response. The heart rate and blood pressure changes during CFT had a longer latency than baroreflex evoked responses. Moreover, one subject had bradycardia despite a fall in blood pressure. The two patients had abnormal Valsalva ratios and no change in heart rate during tilt, indicating impairment of the baroreflex. However, both their heart rate and blood pressure responses to CFT were normal. These data are further evidence of the limited role of the baroreflex in the autonomic responses to CFT. They suggest that the CFT may be of use in assessing the integrity of the efferent cardiovascular autonomic pathways in patients with suspected baroreflex impairment.

Adult↗
PubMed1993

Evaluation of spontaneous baroreflex response after 28 days head down tilt bedrest.

The spontaneous baroreflex response was evaluated during supine rest and head up tilt (60 degrees) before and immediately after a 28 day 6 degrees HDT bedrest in 6 healthy adult men (age 30-42 years). Sequences of 3 or more beats where RR-interval and systolic blood pressure changed in the same direction were used to evaluate baroreflex response slope (BRS). Prior to bedrest, the mean BRS and RR-interval were 18.0 +/- 3.9 ms/mm Hg and 926 +/- 61 ms at rest and 10.5 +/- 2.5 ms/mm Hg and 772 +/- 63 ms during the first 10 min of 60 degrees tilt. Following bedrest, these values changed to 15.6 +/- 2.7 ms/mm Hg and 780 +/- 53 ms at rest, and to 6.5 +/- 1.2 ms/mm Hg and 636 +/- 44 ms during tilt. Thus, (1) the spontaneous baroreflex can be evaluated in human subjects during experiments of orthostatic stress; (2) the baroreflex slope was reduced on going from supine to the head up tilt position; and (3) 28 days of bedrest reduced the spontaneous baroreflex slope.

Adult↗
PubMed1994

Altered frequency-dependent characteristics of the cardiac baroreflex in essential hypertension.

Blood pressure (BP) oscillations contain rhythmic components of low-, mid-, and high-frequency bands (0.02-0.06, 0.07-0.14, 0.15-0.40 Hz, respectively). Baroreceptors may sense each BP oscillation and induce a buffer reaction. To clarify the frequency-dependent baroreflex response and its possible alteration in patients with high BP, both BP (Finapres) and the RR interval (electrocardiogram) were continuously monitored in untreated patients with essential hypertension (EH) (n = 52) and normotensive subjects (NT) (n = 43). The magnitude and phase response of cardiac beats to BP oscillations were examined by transfer function analysis. Spontaneous baroreflex sensitivity was assessed by linear regression analysis of the BP and RR oscillations. The heart rate responded linearly to BP oscillations in more subjects at mid- and high-frequency bands (83% or more) than at the low-frequency band (60% or less). The phase was approximately zero at the high-frequency band and was consistently negative at the mid- and low-frequency bands. In general, all frequency gains were significantly and positively correlated with spontaneous baroreflex sensitivity. Each frequency gain was smaller in EH patients than in NT subjects, the high-frequency gain more so than the gains at the lower frequencies. In seven young EH patients, treatment with a beta 1-adrenoceptor selective blocker normalized the high-frequency gain and tended to increase the gains at the lower frequencies. These results suggest that the spontaneous baroreflex modulates RR oscillations over a broad frequency range from 0.02 to 0.40 Hz; the effect was most marked at frequencies higher than 0.07 Hz. Furthermore the frequency-dependent characteristics of the cardiac baroreflex were altered in essential hypertension partly because of an increased beta-adrenergic activity.

Adrenergic beta-1 Receptor Antagonists↗
PubMed1996

Age-related changes in baroreflex control of heart rate and sympathetic nerve activity in healthy humans.

To determine how the baroreflex control of sympathetic nerve activity is affected by aging, muscle sympathetic nerve activity (MSNA) from the tibial nerve was monitored using microneurography, and heart rate and blood pressure were recorded during the pressor or depressor responses to intravenous injections of phenylephrine or nitroglycerin in 39 healthy humans, aged 16 to 56 years. Although the baroreflex slope for heart rate showed attenuation with aging, the baroreflex slope for MSNA was not affected by aging. These data suggest preservation of the baroreflex control of sympathetic nerve activity despite attenuation of the baroreflex control of parasympathetic nerve activity by aging in humans.

Adolescent↗
PubMed1995

Effects of nitric oxide on sympathetic baroreflex transmission in the nucleus tractus solitarii and caudal ventrolateral medulla in cats.

We have previously shown that nitric oxide (NO) attenuates baseline sympathetic tone in the rostral ventrolateral medulla (RVLM), while having no effects on baroreflex transmission in this region in cats. In the present study, we tested the effects of microinjections (500 nl) of NG-nitro-L-arginine (L-NNA, 0.3 mM) or the NO donor S-nitroso-N-acetylpenicillamine (SNAP, 10 microM) in the nucleus tractus solitarii (NTS) and in the caudal ventrolateral medulla (CVLM) which are the two other relays of the sympathetic baroreflex within the brainstem. Neither L-NNA nor SNAP significantly changed the length of inhibition of renal sympathetic nerve activity (SNA) evoked by electrical stimulation of the ipsilateral carotid sinus nerve. In contrast, glutamate (1 mM) in the NTS markedly increased baroreflex inhibition of SNA and the glutamate receptor antagonist kynurenate (5 mM) in the CVLM significantly decreased baroreflex transmission in the same experiments. These results suggest that sympathetic baroreflex function is preserved during both impaired endogenous synthesis and excess exogenous supply of NO in the brainstem.

Animals↗
PubMed1995

Amino acids in the medulla oblongata contribute to baroreflex modulation by angiotensin II.

We investigated the underlying mechanisms of baroreflex alteration produced by intravenous angiotensin II (ANG II) by monitoring the release of amino acids from the rostral ventrolateral medulla (VLM) using a brain microdialysis technique. Reflex changes in heart rate were elicited by bolus intravenous injection of phenylephrine (2-40 micrograms/kg) before and 120 min after the initiation of administration of a subpressor dose of ANG II (5.4 pmol/kg/min) or vehicle. The slope of the regression line obtained from changes in mean arterial pressure and heart rate elicited by phenylephrine was used as an index of baroreceptor reflex sensitivity. ANG II administration for 120 min significantly attenuated the baroreflex sensitivity (from -0.59 +/- 0.10 to -0.30 +/- 0.08 bpm/mmHg). This attenuation was accompanied with an increase in the release of glutamate and glycine from the VLM (+40% and +20%, respectively) at 120 min. Glycine perfusion into this area resulted in an attenuation of baroreflex sensitivity with a magnitude similar to that obtained with infusion of a subpressor dose of ANG II, whereas glutamate perfusion caused a resetting of baroreflex. These results suggest that glycine and glutamate are involved in cardiovascular regulation in the VLM. Furthermore, the augmented releases of these amino acids may account for the underlying mechanism of ANG II-induced attenuation of baroreflex function.

Amino Acids↗
PubMed1993

Impairment of the arterial baroreflex during symptomatic and silent myocardial ischemia in humans.

OBJECTIVES: The aim of this study was to assess whether transient episodes of symptomatic or silent myocardial ischemia after baroreceptor modulation of heart rate. BACKGROUND: Animal and human studies have shown that myocardial infarction is accompanied by an impairment of the baroreceptor influences on the sinus node. However, whether this also occurs during transient myocardial ischemia has never been documented. METHODS: In 12 patients undergoing coronary angiography, systolic blood pressure (intraarterial catheter) was reduced by an intravenous bolus of nitroglycerin during a spontaneous episode of transient chest pain and myocardial ischemia (ST segment depression on the electrocardiogram) and 30 min after recovery. The slope of the linear regression between the decrease in systolic blood pressure and the RR interval shortening was taken as the measure of baroreflex sensitivity. RESULTS: During ischemia, baroreflex sensitivity was 1.3 +/- 0.3 ms/mm Hg (mean +/- SEM), whereas after recovery it was markedly and significantly greater (2.6 +/- 0.5 ms/mm Hg, p < 0.01). Similar results were obtained in eight other patients who experienced a silent ischemic episode either spontaneously or during coronary angioplasty. The reduction in baroreflex sensitivity was similarly pronounced during inferior (10 patients) and anterior (10 patients) ischemia, and its magnitude showed little or no relation to the ischemia-dependent changes in blood pressure and heart rate. CONCLUSIONS: Transient myocardial ischemia is associated with marked baroreflex impairment. The impairment occurs even during symptomless ischemic episodes and is therefore not related to pain or to other nonspecific influences on the baroreflex.

Baroreflex↗