scholarly journals Spontaneous fluctuation indices of the cardiovagal baroreflex accurately measure the baroreflex sensitivity at the operating point during upright tilt

2013 ◽  
Vol 304 (12) ◽  
pp. R1107-R1113 ◽  
Author(s):  
Christopher E. Schwartz ◽  
Marvin S. Medow ◽  
Zachary Messer ◽  
Julian M. Stewart

Spontaneous fluctuation indices of cardiovagal baroreflex have been suggested to be inaccurate measures of baroreflex function during orthostatic stress compared with alternate open-loop methods (e.g. neck pressure/suction, modified Oxford method). We therefore tested the hypothesis that spontaneous fluctuation measurements accurately reflect local baroreflex gain (slope) at the operating point measured by the modified Oxford method, and that apparent differences between these two techniques during orthostasis can be explained by a resetting of the baroreflex function curve. We computed the sigmoidal baroreflex function curves supine and during 70° tilt in 12 young, healthy individuals. With the use of the modified Oxford method, slopes (gains) of supine and upright curves were computed at their maxima ( Gmax) and operating points. These were compared with measurements of spontaneous indices in both positions. Supine spontaneous analyses of operating point slope were similar to calculated Gmax of the modified Oxford curve. In contrast, upright operating point was distant from the centering point of the reset curve and fell on the nonlinear portion of the curve. Whereas spontaneous fluctuation measurements were commensurate with the calculated slope of the upright modified Oxford curve at the operating point, they were significantly lower than Gmax. In conclusion, spontaneous measurements of cardiovagal baroreflex function accurately estimate the slope near operating points in both supine and upright position.

2013 ◽  
Vol 305 (7) ◽  
pp. H1041-H1049 ◽  
Author(s):  
Vienna E. Brunt ◽  
Jennifer A. Miner ◽  
Paul F. Kaplan ◽  
John R. Halliwill ◽  
Lisa A. Strycker ◽  
...  

The individual effects of estrogen and progesterone on baroreflex function remain poorly understood. We sought to determine how estradiol (E2) and progesterone (P4) independently alter the carotid-cardiac and carotid-vasomotor baroreflexes in young women by using a hormone suppression and exogenous add-back design. Thirty-two young women were divided into two groups and studied under three conditions: 1) after 4 days of endogenous hormone suppression with a gonadotropin releasing hormone antagonist (control condition), 2) after continued suppression and 3 to 4 days of supplementation with either 200 mg/day oral progesterone ( N = 16) or 0.1 to 0.2 mg/day transdermal 17β-estradiol ( N = 16), and 3) after continued suppression and 3 to 4 days of supplementation with both hormones. Changes in heart rate (HR), mean arterial pressure (MAP), and femoral vascular conductance (FVC) were measured in response to 5 s of +50 mmHg external neck pressure to unload the carotid baroreceptors. Significant hormone effects on the change in HR, MAP, and FVC from baseline at the onset of neck pressure were determined using mixed model covariate analyses accounting for P4 and E2 plasma concentrations. Neither P4 ( P = 0.95) nor E2 ( P = 0.95) affected the HR response to neck pressure. Higher P4 concentrations were associated with an attenuated fall in FVC ( P = 0.01), whereas higher E2 concentrations were associated with an augmented fall in FVC ( P = 0.02). Higher E2 was also associated with an augmented rise in MAP ( P = 0.01). We conclude that progesterone blunts whereas estradiol enhances carotid-vasomotor baroreflex sensitivity, perhaps explaining why no differences in sympathetic baroreflex sensitivity are commonly reported between low and high combined hormone phases of the menstrual cycle.


2015 ◽  
Vol 309 (8) ◽  
pp. H1361-H1369 ◽  
Author(s):  
Rachel C. Drew ◽  
Cheryl A. Blaha ◽  
Michael D. Herr ◽  
Sean D. Stocker ◽  
Lawrence I. Sinoway

Low-dose aspirin inhibits thromboxane production and augments the sensitivity of carotid baroreflex (CBR) control of heart rate (HR) during concurrent muscle mechanoreflex and metaboreflex activation in healthy young humans. However, it is unknown how aging affects this response. Therefore, the effect of low-dose aspirin on carotid-cardiac baroreflex sensitivity during muscle mechanoreflex with and without metaboreflex activation in healthy older humans was examined. Twelve older subjects (6 men and 6 women, mean age: 62 ± 1 yr) performed two trials during two visits preceded by 7 days of low-dose aspirin (81 mg) or placebo. One trial involved 3 min of passive calf stretch (mechanoreflex) during 7.5 min of limb circulatory occlusion (CO). In another trial, CO was preceded by 1.5 min of 70% maximal voluntary contraction isometric calf exercise (mechanoreflex and metaboreflex). HR (ECG) and mean arterial blood pressure (MAP; Finometer) were recorded. CBR function was assessed using rapid neck pressure application (+40 to −80 mmHg). Aspirin significantly decreased baseline thromboxane B2 production by 83 ± 4% ( P < 0.05) but did not affect 6-keto-PGF1α. After aspirin, CBR-HR maximal gain and operating point gain were significantly higher during stretch with metabolite accumulation compared with placebo (maximal gain: −0.23 ± 0.03 vs. −0.14 ± 0.02 and operating point gain: −0.11 ± 0.03 vs. −0.04 ± 0.01 beats·min−1·mmHg−1 for aspirin and placebo, respectively, P < 0.05). In conclusion, these findings suggest that low-dose aspirin augments CBR-HR sensitivity during concurrent muscle mechanoreflex and metaboreflex activation in healthy older humans. This increased sensitivity appears linked to reduced thromboxane sensitization of muscle mechanoreceptors, which consequently improves CBR-HR control.


2006 ◽  
Vol 101 (1) ◽  
pp. 68-75 ◽  
Author(s):  
Shigehiko Ogoh ◽  
R. Matthew Brothers ◽  
Quinton Barnes ◽  
Wendy L. Eubank ◽  
Megan N. Hawkins ◽  
...  

The purpose of this investigation was to examine whether the effect of changes in central blood volume on carotid-vasomotor baroreflex sensitivity at rest was the same during exercise. Eight men (means ± SE: age 26 ± 1 yr; height 180 ± 3 cm; weight 86 ± 6 kg) participated in the present study. Sixteen Torr of lower body negative pressure (LBNP) were applied to decrease central venous pressure (CVP) at rest and during steady-state leg cycling at 50% peak O2 uptake (104 ± 20 W). Subsequently, infusions of 25% human serum albumin solution were administered to increase CVP at rest and during exercise. During all protocols, heart rate, arterial blood pressure, and CVP were recorded continuously. At each stage of LBNP or albumin infusion, the maximal gain (Gmax) of the carotid-vasomotor baroreflex function curve was measured using the neck pressure and neck suction technique. LBNP reduced CVP and increased the Gmax of the carotid-vasomotor baroreflex function curve at rest (+63 ± 25%, P = 0.006) and during exercise (+69 ± 19%, P = 0.002). In contrast to the LBNP, increases in CVP resulted in the Gmax of the carotid-vasomotor baroreflex function curve being decreased at rest −8 ± 4% and during exercise −18 ± 5% ( P > 0.05). These findings indicate that the relationship between CVP and carotid-vasomotor baroreflex sensitivity was nonlinear at rest and during exercise and suggests a saturation load of the cardiopulmonary baroreceptors at which carotid-vasomotor baroreflex sensitivity remains unchanged.


1993 ◽  
Vol 265 (6) ◽  
pp. H1928-H1938 ◽  
Author(s):  
J. T. Potts ◽  
X. R. Shi ◽  
P. B. Raven

We utilized 5-s changes of neck pressure and neck suction (from 40 to -80 Torr) to alter carotid sinus transmural pressure in seven men with peak oxygen uptake (VO2peak) of 41.4 +/- 3.6 ml O2.kg-1.min-1. Peak responses of heart rate (HR) and mean arterial pressure (MAP) to each carotid sinus perturbation were used to construct open-loop baroreflex curves at rest and during exercise at 25.7 +/- 1.1 and 47.4 +/- 1.9% VO2peak. The baroreflex curves were fit to a logistic function describing the sigmoidal nature of the carotid sinus baroreceptor reflex. Maximal gain for baroreflex control of HR (-0.31 +/- 0.05 beats.min-1.mmHg-1) and MAP (-0.30 +/- 0.08 mmHg/mmHg) at rest was the same as during exercise at 25 and 50% VO2peak (-0.30 +/- 0.05, -0.39 +/- 0.13 beats.min-1.mmHg-1 for HR, P = NS; -0.23 +/- 0.04, -0.60 +/- 0.38 mmHg/mmHg for MAP, P = NS). Resetting of the baroreflex occurred during exercise at 50% VO2peak. The centering point, threshold, and saturation pressures were significantly increased for baroreflex control of HR (delta pressure = 26.3 +/- 6.8, 19.6 +/- 10.4, 33.0 +/- 5.6 mmHg, P < 0.05) and MAP (delta pressure = 27.1 +/- 7.7, 16.1 +/- 14.8, 38.2 +/- 8.5 mmHg, P < 0.05). The operating point (steady-state HR and MAP) was shifted closer to threshold of the baroreflex during exercise at 50% VO2peak, as reflected by differences in HR and MAP between the centering and operating points (delta HR = 12.5 +/- 4.7 beats/min, P = 0.10; delta MAP = 7.6 +/- 1.3 mmHg, P < 0.05). These findings suggest a resetting of the carotid baroreflex during exercise with no attenuation in maximal sensitivity. A shift in operating point toward threshold of the baroreflex enables effective buffering of elevations in systemic blood pressure via reflex alterations in HR and MAP.


Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Hossam A Shaltout ◽  
John E Fortunato ◽  
Debra I Diz

Fludrocortisone (Florinef) is commonly used to treat symptoms associated with postural orthostatic tachycardia syndrome (POTS). We have previously shown that Florinef treatment in children with POTS improved the changes in baroreflex sensitivity (BRS) and heart rate variability (HRV) measured as the root of mean square of successive differences (rMSSD) during upright tilt compared to untreated children with POTS. We noticed that a subgroup of our patients experienced POTS symptoms followed by syncope at later time points during the 45 min tilt test in both Florinef treated and untreated groups. We stratified based on syncope and compared the effect of Florinef treatment on both groups. Of the 32 POTS patients studied (15.0 ± 0.6 yrs old), 14 were treated with Florinef of whom 5 had syncope, and 18 were untreated of whom 5 had syncope. In the non-syncopal group, subjects treated with Florinef for a minimum of 4 wks compared with untreated POTS without syncope had similar baseline supine measures of MAP, HR, BRS and HRV before tilt, and less reduction in BRS during tilt measured as Seq UP (-7.1 ± 2.5 vs -15.1 ± 3.5 ms/mmHg; p<0.03), a trend for less attenuation in HRV (-22.4 ± 6.4 vs -35.3 ± 6.3 ms; p<0.07) and reduced tachycardia with tilt (25 ± 6 vs 38 ± 4 beats/min; p<0.02) compared with the untreated group. Meanwhile, in the syncopal group, Florinef-treated patients at baseline in the supine position before tilt had worse BRS function measured as Seq UP compared to untreated (11.9 ± 2.2 vs 26.0 ± 6.7 ms/mm Hg; p<0.04), a tendency for lower HRV (40.8 ± 7 vs 61.2 ± 12 ms; p<0.08) and higher HR (82 ± 3 vs 65 ± 7 beats/min; p<0.02) than untreated POTS patients with syncope. In contrast to non-syncopal POTS, the HR increase during tilt in syncopal POTS subjects was not reduced by the Florinef. The impairments in baseline supine autonomic function in POTS with syncope patients treated with Florinef relative to untreated patients and lack of improvement in the performance upon upright tilt suggests that POTS patients should be stratified by syncope status during the tilt test prior to assigning this treatment regimen. Additional studies are needed to better define these patients and to determine if other pharmacologic agents would provide a more optimal treatment. Support: AHA12CRP9420029


Author(s):  
IS Palamarchuk ◽  
J Baker ◽  
K Kimpinski

Background: Valsalva maneuver (VM) is a simple and non-invasive technique extensively utilized clinically to detect dysautonomia. VM provides detailed information of baroreflex sensitivity (BRS) which is an important cardiovascular and autonomic marker. However, the current approach for calculating its adrenergic component (BRSa1) is moderately reliable and fails to evaluate atypical VM patterns. Methods: We analyzed typical and atypical VM patterns of 89 young, healthy individuals (30 ±13 years) with the aim of improving BRSa evaluation. Objectives: 1) To determine a new BRSa calculation (BRSa2) applicable to different VM patterns; 2) correlate BRSa2 to BRSa1; 3) compare the internal consistency (ICC) between BRSa1 and BRSa2. Results: The BRSa2 calculation is a complex hemodynamic and time assessment equivalent to the slope in vagal BRS. In contrast to BRSa1, BRSa2 operates with hemodynamic indices easily detectable in any VM pattern. In atypical VM patterns, BRSa2 correlated with BRSa1: “flat-top responses” (r = 0.774, p < 0.01); rapid hemodynamic recovery (r = 0.461, p < 0.05). Most importantly, BRSa2 was more reliable than BRSa1 (ICC= 0.759 versus 0.469). Conclusion: BRSa2 is more reliable and allows atypical responses to VM to be analyzed, which clinically, could help differentiate natural physiological variances and mild adrenergic dysfunction.


2015 ◽  
Vol 192 ◽  
pp. 109 ◽  
Author(s):  
W.W. Holbein ◽  
J.K. Limberg ◽  
N. Covassin ◽  
M.J. Joyner ◽  
V.K. Somers

1998 ◽  
Vol 76 (4) ◽  
pp. 381-386 ◽  
Author(s):  
Mahmoud M El-Mas ◽  
Abdel A Abdel-Rahman

In previous studies, we have shown that the baroreflex control of heart rate is significantly attenuated in females compared with age-matched males. This study investigated the role of estrogen in the modulation of baroreflex function in conscious unrestrained rats. Baroreflex-mediated decreases in heart rate in response to increments in blood pressure evoked by phenylephrine were evaluated in conscious freely moving male and female Sprague-Dawley rats as well as in ovariectomized rats. The effect of a 2-day 17 beta -estradiol (50 µg ·kg-1 ·day-1, s.c.) or vehicle treatment on baroreflex sensitivity was investigated in ovariectomized rats. Intravenous bolus doses of phenylephrine (1-16 µg/kg) elicited dose-dependent pressor and bradycardic responses in all groups of rats. Regression analysis of the baroreflex curves relating increments in blood pressure to the associated heart rate responses revealed a significantly (p < 0.05) smaller baroreflex sensitivity in female compared with male rats (-1.22 ± 0.07 and -1.85 ± 0.15 beats ·min-1 ·mmHg-1, respectively), suggesting an attenuated baroreflex function in females. In age-matched ovariectomized rats, baroreflex sensitivity showed further reduction (-0.93 ± 0.02 beats ·min-1 ·mmHg-1). Treatment of ovariectomized rats with 17 beta -estradiol significantly (p < 0.05) enhanced the baroreflex sensitivity (-1.41 ± 0.16 beats ·min-1 ·mmHg-1) to a level that was slightly higher than that of sham-operated female rats. Furthermore, baroreflex sensitivity of ovariectomized estradiol-treated rats was not significantly different from that of age-matched male rats. The vehicle, on the other hand, had no effect on baroreflex sensitivity of ovariectomized rats. These data support our earlier findings that sexual dimorphism exists in baroreflex control of heart rate. More importantly, the present study provides experimental evidence that suggests a facilitatory role for estrogen in the modulation of baroreflex function.Key words: rat, gender, baroreflex sensitivity, 17 beta -estradiol, ovariectomy.


2012 ◽  
Vol 302 (10) ◽  
pp. H1991-H1997 ◽  
Author(s):  
Jason R. Carter ◽  
John J. Durocher ◽  
Robert A. Larson ◽  
Joseph P. DellaValla ◽  
Huan Yang

Sleep deprivation has been linked to hypertension, and recent evidence suggests that associations between short sleep duration and hypertension are stronger in women. In the present study we hypothesized that 24 h of total sleep deprivation (TSD) would elicit an augmented pressor and sympathetic neural response in women compared with men. Resting heart rate (HR), blood pressure (BP), and muscle sympathetic nerve activity (MSNA) were measured in 30 healthy subjects (age, 22 ± 1; 15 men and 15 women). Relations between spontaneous fluctuations of diastolic arterial pressure and MSNA were used to assess sympathetic baroreflex function. Subjects were studied twice, once after normal sleep and once after TSD (randomized, crossover design). TSD elicited similar increases in systolic, diastolic, and mean BP in men and women (time, P < 0.05; time × sex, P > 0.05). TSD reduced MSNA in men (25 ± 2 to 16 ± 3 bursts/100 heart beats; P = 0.02), but not women. TSD did not alter spontaneous sympathetic or cardiovagal baroreflex sensitivities in either sex. However, TSD shifted the spontaneous sympathetic baroreflex operating point downward and rightward in men only. TSD reduced testosterone in men, and these changes were correlated to changes in resting MSNA ( r = 0.59; P = 0.04). Resting HR, respiratory rate, and estradiol were not altered by TSD in either sex. In conclusion, TSD-induced hypertension occurs in both sexes, but only men demonstrate altered resting MSNA. The sex differences in MSNA are associated with sex differences in sympathetic baroreflex function (i.e., operating point) and testosterone. These findings may help explain why associations between sleep deprivation and hypertension appear to be sex dependent.


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