Carotid-cardiac baroreflex function does not influence blood pressure regulation during head-up tilt in humans

The influence of the carotid-cardiac baroreflex on blood pressure regulation was evaluated during supine rest and 40 degrees head-up tilt (HUT) in 9 healthy young subjects with and without full cardiac vagal blockade. The carotid baroreflex responsiveness, or maximal gain (G(MAX)), was assessed from the beat-to-beat changes in heart rate (HR) and mean arterial pressure (MAP) by the variable neck pressure and suction technique ranging in pressure from +40 to -80 Torr, with and without glycopyrrolate (12.0 +/- 1.0 microg/kg body weight; mean +/- SE). In the supine position, glycopyrrolate increased the HR to 91 +/- 3 bpm, from 54 +/- 3; MAP to 89 +/- 2 mmHg, from 76 +/- 2; and cardiac output to 6.8 +/- 0.3 l.min(-1), from 4.9 +/- 0.3 (P < 0.05). The G(MAX) of the carotid baroreflex control of HR was reduced to -0.06 +/- 0.01 bpm.mmHg(-1), from -0.30 +/- 0.02 (P < 0.05) with no significant effect on the G(MAX) of the carotid baroreflex control of MAP. During HUT the carotid baroreflex control of MAP was unchanged, though the G(MAX) of the carotid baroreflex control of HR was increased (P < 0.05). During HUT, central blood volume, assessed by electrical thoracic admittance, and total vascular conductance were decreased with and without glycopyrrolate. Furthermore, glycopyrrolate reduced G(MAX) of the carotid baroreflex control of HR during HUT (P < 0.05) with no significant effect on G(MAX) of the carotid baroreflex control of MAP. These data suggest that during supine rest and HUT-induced decreases in central blood volume, the carotid baroreflex control of HR is mediated primarily via parasympathetic activity. Furthermore, the maintenance of arterial blood pressure during postural stress is primarily mediated by arterial and cardiopulmonary reflex regulation of sympathetic activity and its effects on the systemic vasculature.     

Thermal stress modulates arterial pressure variability and arterial baroreflex response of heart rate during head-up tilt in humans

To examine the effects of thermal stress on the blood pressure variability and the arterial baroreceptor-cardiac reflex during orthostatic stress, 11 male volunteers underwent whole body thermal stress using a cool or hot water-perfused suit during 5 min of 70° head-up tilt (HUT). The spontaneous variability in arterial pressure was quantified by power spectrum analysis. The sensitivity of the arterial baroreceptor-cardiac reflex was calculated from the spontaneous changes in beat-to-beat arterial pressure and heart rate (f _c). During supine rest the variability of arterial pressure decreased during cooling, while it remained unchanged during heating. The variability increased with HUT; it was greater (P<0.05) with heating than with cooling. In the supine condition, the arterial baroreflex sensitivity of f _c increased during cooling, while it did not change during heating. The sensitivities decreased (P<0.05) with HUT during both thermal stresses; the decreased rate of sensitivity from the pre-tilt value was greater during heating [mean 63 (SEM 4)%] and smaller during cooling [mean 11 (SEM 24)%] than during normothermia [mean 47 (SEM 4)%] (both, P<0.05). There were significant negative correlations between the sensitivities and the amplitude of the arterial pressure variability during normothermia and heating (P<0.0001). The results suggest that the spontaneous baroreflex response of f _c is a modulatory factor for the changes of arterial pressure variability brought about by thermal stress during orthostatic stress. Electronic Publication     

Model-based assessment of baroreflex and cardiopulmonary couplings during graded head-up tilt

We propose a multivariate dynamical adjustment (MDA) modeling approach to assess the strength of baroreflex and cardiopulmonary couplings from spontaneous cardiovascular variabilities. Open loop MDA (OLMDA) and closed loop MDA (CLMDA) models were compared. The coupling strength was assessed during progressive sympathetic activation induced by graded head-up tilt. Both OLMDA and CLMDA models suggested that baroreflex coupling progressively increased with tilt table inclination. Only CLMDA model indicated that cardiopulmonary coupling due to the direct link from respiration to heart period gradually decreased with tilt table angles, while that due to the indirect link mediated by systolic arterial pressure progressively increased.     

Sympathetic influence on cardiovascular responses to sustained head-up tilt in humans

Sympathetic β-adrenergic influences on cardiovascular responses to 50d? head-up tilt were evaluated with metoprolol (β₁-blockade; 0.29 mg kg^-1) and propranolol (β₁ and β-₂-blockade; 0.28 mg kg^-1) in eight males. A normotensive-tachycardic phase was followed by a hypotensive-bradycardic episode associated with presyncopal symptoms after 23pL3 min (control, mean pLSE). Head-up tilt made thoracic electrical impedance (3.0pL10Ω), mean arterial pressure (MAP, 86pL4-93pL4 mmHg), heart rate (HR, 63pL3-99pL10 beats min^-1) and total peripheral resistance (TPR, 15pL1-28pL4 mmHg min L^-1) increase, while central venous oxygen saturation (74pL2-58pL4%), cardiac output (5.7pL0.1–3.1pL0.3 L min^-1), stroke volume (95pL6-41pL5 mL) and pulse pressure (55pL4-49pL4 mmHg) decreased (P < 0.05). Central venous pressure decreased during head-up tilt (7pL2-0pL1 mmHg), but it remained stable during the sustained tilt. At the appearance of preswyncopal symptoms MAP (49pL3 mmHg), HR (66pL4 beats min^-1) and TPR (15pL3 mmHg min L^-1) decreased (P < 0.05). Neither metoprolol or propranolo changed tilt tolerance or cardiovascular variables, except for HR that remained at 57pL2 (metoprolol) and 55pL3 beats min^-1 (propranolol), and MAP that remained at 87pL5 mmHg during the first phase with metoprolol. In conclusion, sympathetic activation was crucial for the heart rate elevation during normotensive head-up tilt, but not for tilt tolerance or for the associated hypotension and bradycardia.     

Effect of diazepam on endocrine and cardiovascular responses to head-up tilt in humans

Effects of the GABAergic drug diazepam (0.15 mg kg^-1, i.v.) on cardiovascular and endocrine responses to 50± head-up tilt were evaluated in seven men. During the initial phase of tilt (normotensive phase), increases in heart rate (HR) and total peripheral resistance (TPR) and decreases in cardiac output were unaffected by diazepam. Also the associated increase in plasma noradrenaline did not change, while response in plasma ACTH was diminished and in plasma cortisol abolished by diazepam (F(1, 10) = 6.45; P < 0.03). After 42 ± 4 min of sustained tilt with saline (control) and 47 ± 6 min (n.s.) after diazepam, presyncopal symptoms appeared (hypotensive phase) associated with decreases in HR, MAP, and TPR (P < 0.01). This episode induced a 2–3-fold increase in plasma ACTH, β-endorphin, prolactin, cortisol (< 0.01), and a moderate increase in plasma adrenaline (P < 0.05). Diazepam did not significantly change cardiovascular and endocrine responses to the hypotensive phase of tilt. Results indicate that diazepam attenuates the cortisol part of pituitary-adrenal responses to moderate, but not to severe, central hypovolaemia in humans with no effect on cardiovascular tolerance.     

Influence of Naloxone on the cellular immune response to head-up tilt in humans

To evaluate a possible role for β-endorphin in the stress-induced modulation of natural killer (NK) cells, immunologically competent blood cells were followed in eight male volunteers administered either Naloxone or saline (control) during head-up tilt maintained until the appearance of presyncopal symptoms (PS). The PS appeared more rapidly with Naloxone compared to control [5.7 (SEM 1.1) vs 22.3 (SEM 5.1) min; P?=?0.01]. The NK cell activity increased threefold during PS partly due to an increase in CD16⁺ and CD56⁺ NK cells in blood. In support, NK cell activity boosted with interferon-α and interleukin 2 rose in parallel with unboosted NK cell activity and NK cell concentration and activities returned to the baseline level after 105?min. The total lymphocyte count and the concentrations of CD3⁺, CD4⁺, CD8⁺, CD16⁺, and CD56⁺ cells increased during PS. Head-up tilt also induced an increase in plasma adrenaline concentration during control PS and a rise in plasma cortisol and adrenocorticotropic hormone concentrations up to 30?min thereafter, whereas no significant changes were found in plasma concentrations of noradrenaline, growth hormone, or β-endorphin. The results would indicate an influence of endorphin on the increase in plasma adrenaline concentration during head-up tilt and at the same time contra-indicate a significant role for adrenaline in the provocation of PS. The influence of head-up tilt on plasma β-endorphin was too small to influence the modulation of the cellular immune system.     

Age-related effects of vagotonic atropine on cardiovagal baroreflex gain

Impaired neural transduction of barosensory vessel stretch into vagal outflow is a primary determinant of reduced cardiovagal baroreflex gain with human aging. We set out to determine whether age-related reductions in this neural component of the baroreflex might be offset by enhancing the central integration/efferent responsiveness of the neural arc. Low vagotonic doses of atropine were employed to enhance central neural outflow and peripheral sinus node effects. Baroreflex gain and its neural and mechanical components were pharmacologically assessed before and after intravenous vagotonic atropine in 16 older and 14 young healthy subjects. Vagotonic atropine increased cardiovagal baroreflex gain (∼30%) and its neural component (∼20%) in older but not young individuals. Moreover, the atropine-induced increases in integrated gain and in its neural component were inversely related to baseline levels. Thus, age-related neural deficits in the baroreflex arc appear to play a determining role in reduced cardiovagal baroreflex gain with age and the compromised neural baroreflex function can be acutely improved by a single pharmacologic intervention.     

Fluctuations in carotid arterial distensibility during the menstrual cycle do not influence cardiovagal baroreflex sensitivity

Aim: Fluctuations in autonomic nervous functions throughout the menstrual cycle and the underlying mechanism concerning them are not well known. This study was designed to test the hypothesis that fluctuations in cardiovagal baroreflex sensitivity (BRS) throughout the menstrual cycles of young women are due to fluctuations in carotid arterial distensibility. Methods: In eight eumenorrhoeic healthy young women (18–24 years), we determined the variations in the carotid arterial distensibility coefficient (DC; via simultaneous ultrasonography and applanation tonometry), cardiovagal BRS (phase IV of the Valsalva manoeuvre and the sequence method; up‐ or down‐sequence spontaneous BRS), and serum oestradiol and progesterone concentrations at five points in the menstrual cycle (menstrual = M, follicular = F, ovulatory = O, early luteal = EL, and late luteal = LL). Results: Serum oestradiol and progesterone levels were consistent with the predicted cycle phases. Carotid arterial DC fluctuated cyclically, increasing significantly from the M (52.4 ± 4.9 × 10^?3 kPa^?1, mean ± SE) and F (52.7 ± 4.4) phases to the O (57.6 ± 4.4) phase and declining sharply in the EL (46.0 ± 4.0) and LL (45.1 ± 3.0) phases (F = 6.37, P < 0.05). Contrary to our prediction, however, cardiovagal BRS by the Valsalva manoeuvre (P = 0.73) or sequence method (up‐sequence spontaneous BRS; P = 0.84: down‐sequence spontaneous BRS; P = 0.67) did not change significantly during the menstrual cycle. Conclusion: The results suggest that, although carotid arterial distensibility fluctuates with the changes in ovarian hormone levels that occur during the menstrual cycle, the fluctuations in carotid arterial distensibility do not influence cardiovagal BRS.     

An electrical admittance based index of thoracic intracellular water during head-up tilt in humans

During 50° head-up tilt (HUT), the number of erythrocytes within the thorax has been shown to be reduced by approximately 25% and this level is retained during a maintained tilt, whilst that in the thigh increases by approximately 70%. To evaluate whether the electrical admittance of intracellular water (ICW) may be used to monitor this redistribution of red cells in humans, we determined the regional difference in the reciprocal value of the impedance at 1.5 and 100 kHz for the thorax (thorax_ICW) and for the leg (leg_ICW). In ten subjects all variables remained unchanged during head-down tilt but during HUT, presyncopal symptoms were induced in eight subjects after a mean of 27 (SEM 7) min as mean heart rate dropped from 85 (SEM 4) to 66 (SEM 3) beats · min⁻¹, mean arterial blood pressure from 80 (SEM 3) to 60 (SEM 5) mmHg, and mean oxygen saturation of venous blood from 76 (SEM 2)% to 73 (SEM 3)% (P < 0.05). The mean haematocrit increased from 50 (SEM 5)% to 52.5 (SEM 3.5)% (P < 0.01) and mean central venous pressure decreased during tilting (from a mean of 1 (SEM 1) to a mean of −1 (SEM 1) mmHg; P < 0.05) and returned to value at rest during the maintained tilt. Mean thoracic impedances increased by 7.0 (SEM 1.0) Ω (1.5 kHz) and 5.4 (SEM 1.2) Ω (100 kHz), and mean leg impedances decreased by 9.3 (SEM 1.2) Ω (1.5 kHz) and 3.1 (SEM 1.0) Ω (100 kHz) (P < 0.01). Mean thorax_ICW decreased at 40° HUT and remained reduced by 11 (SEM 2) S · 10⁻⁴ (P < 0.05) until the presyncopal symptoms developed, at which time it was lower by 16 (SEM 2) S · 10⁻⁴ (P < 0.01). Mean leg_ICW increased from 97 (SEM 15) to 99 (SEM 15) S · 10⁻⁴ (P=0.08) during HUT but decreased during maintained tilt (to 94 (SEM 15) S · 10⁻⁴; P < 0.05). The results suggested that during HUT, the difference in electrical admittance at a high and a low frequency current reflects the reduced number of red cells within the thorax. Accepted: 10 July 2000     

An electrical admittance based index of thoracic intracellular water during head-up tilt in humans

During 50 degrees head-up tilt (HUT), the number of erythrocytes within the thorax has been shown to be reduced by approximately 25% and this level is retained during a maintained tilt, whilst that in the thigh increases by approximately 70%. To evaluate whether the electrical admittance of intracellular water (ICW) may be used to monitor this redistribution of red cells in humans, we determined the regional difference in the reciprocal value of the impedance at 1.5 and 100 kHz for the thorax (thoraxICW) and for the leg (legICW). In ten subjects all variables remained unchanged during head-down tilt but during HUT, presyncopal symptoms were induced in eight subjects after a mean of 27 (SEM 7) min as mean heart rate dropped from 85 (SEM 4) to 66 (SEM 3) beats x min(-1), mean arterial blood pressure from 80 (SEM 3) to 60 (SEM 5) mmHg, and mean oxygen saturation of venous blood from 76 (SEM 2)% to 73 (SEM 3)% (P < 0.05). The mean haematocrit increased from 50 (SEM 5)% to 52.5 (SEM 3.5)% (P < 0.01) and mean central venous pressure decreased during tilting (from a mean of 1 (SEM 1) to a mean of -1 (SEM 1) mmHg; P < 0.05) and returned to value at rest during the maintained tilt. Mean thoracic impedances increased by 7.0 (SEM 1.0) ohms (1.5 kHz) and 5.4 (SEM 1.2) ohms (100 kHz), and mean leg impedances decreased by 9.3 (SEM 1.2) ohms (1.5 kHz) and 3.1 (SEM 1.0) ohms (100 kHz) (P < 0.01). Mean thoraxICW decreased at 40 degrees HUT and remained reduced by 11 (SEM 2) S x 10(-4) (P < 0.05) until the presyncopal symptoms developed, at which time it was lower by 16 (SEM 2) S x 10(-4) (P < 0.01). Mean legICW increased from 97 (SEM 15) to 99 (SEM 15) S x 10(-4) (P = 0.08) during HUT but decreased during maintained tilt (to 94 (SEM 15) S x 10(-4); P < 0.05). The results suggested that during HUT, the difference in electrical admittance at a high and a low frequency current reflects the reduced number of red cells within the thorax.     

Thoracic impedance and pulmonary atrial natriuretic peptide during head-up tilt induced hypovolaemic shock in humans

Head up and down tilts were used for manipulating the central blood volume in eight volunteers. During head-up tilt thoracic electrical impedance (TI) increased from 36.7 (33.9–52.1) ohm (mean and range) to 41.9 (36.9–59.2) ohm, heart rate from 60 (49–72) to 80 (65–90) beats min^-1 (P < 0.05) and decreased again to 57 (48–67) beats min^-1 accompanying a fall in mean arterial pressure from 86 (76–97) to 54 (41–79) mmHg and in cardiac output from 9.2 (5.9–12.1) to 6.9 (3.4–8.8) 1 min-¹ (n= 7, P < 0.07). Central venous pressure did not change significantly. Pulmonary arterial mean, 6 (3–12) mmHg, and wedge pressures, 4 (1–9) mmHg, decreased to 4 (1–11) and 1 (0–7) mmHg, respectively, and mixed, 78 (77–79%), and central venous oxygen saturations, 72 (71–73)%, fell to 62 (46–75) and 54 (44–58)%, respectively (P < 0.05). Atrial natriuretic peptide (ANP) was determined from blood of the superior vena cava and pulmonary and brachial arteries. Pulmonary artery ANP, 18.4 (7.5–30.7) pmol l^-1, was higher than in vena cava, 13.3 (5.2–20.9) pmol 1^_1 (P < 0.05). At the time of presyncope, pulmonary artery ANP decreased from 20.8 (37.4–10.1) to 13.7 (19.7-5.7) pmol l^-1, in vena cava from 13.8 (23.1–7.1) to 10.2 (17.9-6.7) pmol l^-‘ and in the brachial artery from 16.9 (34.1–5.2) to 11.3 (18.5-5.1) pmol l“¹ (P < 0.05). Head-down tilt did not affect the recorded variables significantly. Thoracic electrical impedance, pulmonary artery pressure and venous oxygen saturations were sensitive indices of the central blood volume as reflected in the release of atrial natriuretic peptide from the right side of the heart.     

Spontaneous arterial baroreflex control of the heart rate during head-down tilt in heat-stressed humans

The purpose of this study was to elucidate the effect of raised body temperature per se during acute heat stress on the spontaneous arterial baroreflex control of heart rate (f _c) in humans. To investigate whether unloading of cardiopulmonary baroreceptors during whole-body heating would alter the arterial baroreflex control of f _c, we controlled loading of the cardiopulmonary baroreceptors by head-down tilt (HDT) at angles of 5°, 10°, 15°, and 30° during heat stress produced by hot-water-perfused suits. The sensitivity of the arterial baroreceptor-cardiac reflex was calculated from the spontaneous changes in beat-to-beat arterial pressure and f _c. As an index of cardiopulmonary baroreceptor loading, the left atrial diameter (LAD) was measured by echocardiography. During whole-body heating, the LAD decreased with the rising body core temperature and increased with the HDT. The decreased LAD during heating almost recovered to the normothermic control level by 10° HDT. In the supine position, cardiac baroreflex sensitivity remained unchanged during heating. Arterial pressure, f _c and cardiac baroreflex sensitivity were not changed by HDT ranging from 5° to 30° during heating. These results suggest that cardiac baroreflex sensitivity remain unchanged during graded loading of the cardiopulmonary baroreceptors in heat-stressed humans. Also, we conclude that the sensitivity of the spontaneous arterial baroreflex controlling the f _c is not influenced by raised body temperature per se during acute heat stress. Electronic Publication     

人体头高位倾斜时的血压变化

目的观察体位改变时不同的血压变化，并探讨其原因。方法将39名受试者分成3组：正常青年组12名，正常老年组11名，帕金森病组16名，采用HRV＆BRS无创伤测定仪（型号SMUP-E），连续记录受试者从仰卧位（Supine）到头高位倾斜（head-up tilt，HUT，＋75°）的血压、心率和血压变异性的变化。结果约59％受试者在倾斜过程中，血压先降低，然后逐步恢复；约33.3％受试者血压无明显变化：另有7．7％受试者在倾斜过程中血压不降反升。青年组中体位改变后血压无明显变化者心率增加百分比（20．69％±6．59％）明显高于血压下降者（8．99％±7．35％，P〈0．05），老年组也有相似的趋势，但无统计学意义，帕金森病组则无规律性。结论体位改变后，血压下降、血压无明显变化、血压上升都有可能发生，其结果取决于不同人群回心血量减少和交感神经兴奋这两者之间的平衡。     

Effects of skin surface cooling and heating on autonomic nervous activity and baroreflex sensitivity in humans

The influence of skin surface cooling and heating on heart rate variability (HRV), blood pressure variability (BPV), and baroreflex sensitivity (BRS) were studied in 11 healthy supine volunteers in air temperatures of 18 degrees C (cool), 24 degrees C (mild), 48 degrees C (warm), and 60 degrees C (hot) in a styrene foam chamber. The high-frequency component of HRV (HFRR) decreased and the ratio of low- to high-frequency components, LFRR/HFRR, increased with skin surface heating. Therefore, a suppression of cardiac vagal nervous activity and an enhancement of cardiac sympathetic nervous activity can be caused by skin surface heating. The low-frequency component of BPV (LFSBP), i.e. the fluctuations of the Mayer waves, increased with skin surface heating. The responses between the very low-frequency components of HRV (VLFRR) and systolic BPV (VLFSBP) to thermal skin stimulation were different, although these variables both were considered to be indicators of the thermoregulatory vasomotor control or renin-angiotensin system. Baroreflex sensitivity (BRS) did not increase with skin surface heating, at least in humans.     

Naloxone-provoked vaso-vagal response to head-up tilt in men

A double-blind paired protocol was used to evaluate, in eight male volunteers, the effects of the endogenous opiate antagonist naloxone (NAL; 0.05 mg· kg^–1) on cardiovascular responses to 50° head-up tilt-induced central hypovolaemia. Progressive central hypovolaemia was characterized by a phase of normotensive-tachycardia followed by an episode of hypotensive-bradycardia. The NAL shortened the former from 20 (8–40) to 5 (3–10) min (median and range; (P < 0.02). Control head-up tilt increased the means of thoracic electrical impedance [from 35.8 (SEM 2.1) to 40.0 (SEM 1.8) ; P < 0.01 of heart rate [HR; from 67 (SEM 5) to 96 (SEM 8) beats · min^–1, P < 0.02], of total peripheral resistance [TPR; from 25.5 (SEM 3.2) to 50.4 (SEM 10.5)mmHg min 1^–1,P < 0.05] and of mean arterial pressure [MAP; from 96 (SEM 2) to 101 (SEM 2)mmHg, P < 0.02]. Decreases were observed in stroke volume [from 65 (SEM 12) to 38 (SEM 9) ml, P < 0.01], in cardiac output [from 3.7 (SEM 0.7) to 2.5 (SEM 0.5) 1 · mint, P < 0.01], in pulse pressure [from 55 (SEM 4) to 37 (SEM 3)mmHg, P < 0.01] and in central venous oxygen saturation [from 73 (SEM 2) to 59 (SEM 4)%, P < 0.01]. During NAL, mean HR increased from 70 (SEM 3); n.s. compared to control) to only 86 (SEM 9) beats · min^–1 (P < 0.02 compared to control) and MAP remained stable. The episode of hypotensive-bradycardia appeared as mean control HR decreased to 77 (SEM 7)beats · min^–1, TPR to 31.4(SEM 7.7)mmHg · min · 1^–1 and MAP to 60 (SEM 5)mmHg (P < 0.01), and the volunteers were tilted supine. Cardiovascular effects of naloxone on central hypovolaemia included a reduced elevation of HR and blood pressures and provocation of the episode of hypotensive-bradycardia.     

Evening binge alcohol disrupts cardiovagal tone and baroreflex function during polysomnographic sleep

Study ObjectivesBinge alcohol consumption is associated with increased cardiovascular risk. The effects of evening binge alcohol consumption (i.e. 4–5 beverages within 2 h) on the vagal components of HRV and cardiovagal baroreflex sensitivity (cvBRS) during sleep remain largely equivocal. The present study examined the effects of evening binge alcohol consumption on nocturnal cardiac vagal tone and baroreflex sensitivity during stage N2, slow wave (SWS), and rapid eye movement (REM) sleep. We hypothesized that evening binge drinking would reduce HRV and cvBRS in each sleep stage.MethodsFollowing a familiarization night within the laboratory, twenty-three participants were examined following a night of binge alcohol consumption and a fluid control (randomized, crossover design). A quality nocturnal beat-to-beat blood pressure signal was obtained in both conditions in 16 participants (seven men, nine women; 25 ± 1 years).ResultsBinge drinking reduced both the high frequency (HF) and time-domain components (i.e. pNN50 and RMSSD) of HRV in stage N2 sleep, SWS, and REM. In addition, cvBRS up-up (vagal activation) was reduced following binge alcohol consumption in stage N2 (21 ± 3 vs. 15 ± 3 ms/mmHg, p = 0.035) and REM (15[11–28] vs. 11[9–18] ms/mmHg, p = 0.009). Binge alcohol consumption reduced cvBRS down-down (vagal withdrawal) in stage N2 (23 ± 2 vs. 14 ± 2 ms/mmHg, p < 0.001), SWS (20[14–30] vs. 14[9–17] ms/mmHg, p = 0.022), and REM (14[11–24] vs. 10[7–15] ms/mmHg, p = 0.006).ConclusionsEvening binge alcohol consumption disrupts cardiac vagal tone and baroreflex function during nearly all sleep stages. These findings provide mechanistic insight into the potential role of binge drinking and alcohol abuse on cardiovascular risk.Clinical Trials DetailsAlcohol and Neural Cardiovascular Control in Binge Drinkers, www.clinicaltrials.gov/ct2/show/{"type":"clinical-trial","attrs":{"text":"NCT03567434","term_id":"NCT03567434"}}NCT03567434, {"type":"clinical-trial","attrs":{"text":"NCT03567434","term_id":"NCT03567434"}}NCT03567434.