Carotid-cardiac Baroreflex Research Articles

PERSONALIZED EXERCISE TRAINING PROGRAM AS A COUNTERMEASURE TO ORTHOSTATIC INTOLERANCE AFTER SPACE FLIGHTS.

PERSONALIZED EXERCISE TRAINING PROGRAM AS A COUNTERMEASURE TO ORTHOSTATIC INTOLERANCE AFTER SPACE FLIGHTS.

Healthy older humans exhibit augmented carotid-cardiac baroreflex sensitivity with aspirin during muscle mechanoreflex and metaboreflex activation

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.

Effect of posture on heart rate control prior to and following dynamic leg exercise (881.8)

Reflex control of cardiovascular function is paramount in maintaining homeostasis both before and after exercise. We investigated the influence of posture on arterial baroreflex function both before and after prolonged moderate to high intensity exercise.9 healthy subjects (1 female) aged 24.4 years (±1.16) volunteered for protocol 1 of the study and 13 healthy subjects (3 female) aged 25.5 years (±0.88) volunteered for protocol 2. Each subject underwent graded exercise test either upright (UR) (protocol 1) or semi‐recumbent (SR) (protocol 2). During both protocols 1 and 2 neck pressure/neck suction protocols were performed at rest, exercising HRs of 120 and 150 bpm, and recovery. Reflex data for HR and MAP were analyzed and baroreflex curves were calculated. Repeated measure ANOVAs was performed and Neuman‐Keuls post hoc analysis was used when differences were detected. Significance was set at P&lt;0.05.Significant differences were identified in operating point values of HR between SR and UR at rest (P&lt;0.001), and between rest and recovery in both SR and UR (p&lt;0.001). Differences were also identified in Carotid‐cardiac baroreflex response range and maximum gain between and within all conditions (p&lt;0.05).Differences in the neural reflexive control of HR at rest and during recovery are related to postural changes in cardiopulmonary loading.Grant Funding Source: Supported by TACSM SRDA

Aspirin augments carotid-cardiac baroreflex sensitivity during muscle mechanoreflex and metaboreflex activation in humans

Muscle mechanoreflex activation decreases the sensitivity of carotid baroreflex (CBR)-heart rate (HR) control during local metabolite accumulation in humans. However, the contribution of thromboxane A2 (TXA2) toward this response is unknown. Therefore, the effect of inhibiting TXA2 production via low-dose aspirin on CBR-HR sensitivity during muscle mechanoreflex and metaboreflex activation in humans was examined. Twelve young subjects performed two trials during two visits, preceded by 7 days' low-dose aspirin (81 mg) or placebo. One trial involved 3-min passive calf stretch (mechanoreflex) during 7.5-min limb circulatory occlusion (CO). In another trial, CO was preceded by 1.5 min of 70% maximal voluntary contraction isometric calf exercise to accumulate metabolites during CO and stretch (mechanoreflex and metaboreflex). HR (ECG) and mean arterial pressure (Finometer) were recorded. CBR function was assessed using rapid neck pressures ranging from +40 to -80 mmHg. Aspirin significantly decreased baseline thromboxane B2 production by 84 ± 4% (P < 0.05) but did not affect 6-keto prostaglandin F1α. Following aspirin, stretch with metabolite accumulation significantly augmented maximal gain (GMAX) and operating point gain (GOP) of CBR-HR (GMAX; -0.71 ± 0.14 vs. -0.37 ± 0.08 and GOP; -0.69 ± 0.13 vs. -0.35 ± 0.12 beats·min(-1)·mmHg(-1) for aspirin and placebo, respectively; P < 0.05). CBR-HR function curves were reset similarly with aspirin and placebo during stretch with metabolite accumulation. In conclusion, these findings suggest that low-dose aspirin augments CBR-HR sensitivity during concurrent muscle mechanoreflex and metaboreflex activation in humans. This increased sensitivity appears linked to reduced TXA2 production, which likely plays a role in metabolite sensitization of muscle mechanoreceptors.

Enhanced open-loop but not closed-loop cardiac baroreflex sensitivity during orthostatic stress in humans

The neural interaction between the cardiopulmonary and arterial baroreflex may be critical for the regulation of blood pressure during orthostatic stress. However, studies have reported conflicting results: some indicate increases and others decreases in cardiac baroreflex sensitivity (i.e., gain) with cardiopulmonary unloading. Thus the effect of orthostatic stress-induced central hypovolemia on regulation of heart rate via the arterial baroreflex remains unclear. We sought to comprehensively assess baroreflex function during orthostatic stress by identifying and comparing open- and closed-loop dynamic cardiac baroreflex gains at supine rest and during 60° head-up tilt (HUT) in 10 healthy men. Closed-loop dynamic "spontaneous" cardiac baroreflex sensitivities were calculated by the sequence technique and transfer function and compared with two open-loop carotid-cardiac baroreflex measures using the neck chamber system: 1) a binary white-noise method and 2) a rapid-pulse neck pressure-neck suction technique. The gain from the sequence technique was decreased from -1.19 ± 0.14 beats·min(-1)·mmHg(-1) at rest to -0.78 ± 0.10 beats·min(-1)·mmHg(-1) during HUT (P = 0.005). Similarly, closed-loop low-frequency baroreflex transfer function gain was reduced during HUT (P = 0.033). In contrast, open-loop low-frequency transfer function gain between estimated carotid sinus pressure and heart rate during white-noise stimulation was augmented during HUT (P = 0.01). This result was consistent with the maximal gain of the carotid-cardiac baroreflex stimulus-response curve (from 0.47 ± 0.15 beats·min(-1)·mmHg(-1) at rest to 0.60 ± 0.20 beats·min(-1)·mmHg(-1) at HUT, P = 0.037). These findings suggest that open-loop cardiac baroreflex gain was enhanced during HUT. Moreover, under closed-loop conditions, spontaneous baroreflex analyses without external stimulation may not represent open-loop cardiac baroreflex characteristics during orthostatic stress.

Sex Differences In Carotid Baroreflex Control Of Heart Rate At Rest And During Dynamic Exercise In Humans

Previous studies in animals have demonstrated that the arterial baroreflex control of heart rate (HR) was greater in female compared to male rodents. In contrast, equivocal results have been reported in humans with several studies reporting that young women, in fact, exhibit a reduced cardiac baroreflex sensitivity compared to young men. In addition, to date, no studies have examined differences in the baroreflex control of HR during exercise in young men and women. PURPOSE: To determine if the carotid baroreflex control of HR differs between young men and women at rest or during dynamic exercise. METHODS: Beat-to-beat HR and blood pressure were measured in nine young women (22±1 yr) and men (22±1 yr) at rest and during steady-state leg cycling at 50% HR reserve. All women were studied during the early follicular phase of the menstrual cycle (days 2-5). Five second pulses of neck suction (NS, -60 Torr) and neck pressure (NP, + 40 Torr) were applied to selectively load and unload the carotid baroreceptors, respectively. In addition, HR variability analyses were employed to investigate time and frequency domain indices of parasympathetic and sympathetic control of HR. RESULTS: At rest and during exercise, HR responses to NS were significantly greater in women than men (rest, D -16±3 women vs. D -8±1 men bpm, P = 0.002; exercise, D -17±3 women vs. D -6±1 men bpm, P = 0.004), whereas responses to NP were similar between groups (rest, D + 7±1 women vs. D + 5±1 men bpm, P = 0.222; exercise, D + 4±1 women vs. D + 2±1 men bpm, P = 0.096). In addition, there were no differences in HR variability measurements between women and men both at rest and during exercise. CONCLUSION: Carotid baroreflex mediated HR responses to a hypertensive challenge are greater in young women both at rest and during exercise. In contrast, the ability of the carotid-cardiac baroreflex to respond to a hypotensive challenge is similar between young women and men. Overall, these preliminary data suggest that sex differences in cardiac baroreflex responses are selective to hypertensive challenges both at rest and during exercise.

Interaction of the muscle mechanoreflex and graded metaboreflex activation in reducing carotid‐cardiac baroreflex gain in man.

We have shown that muscle mechanoreflex stimulation during concurrent metaboreflex activation reduces maximal gain (Gmax) of the carotid‐cardiac baroreflex in man. The effect of graded metabolite accumulation and metaboreflex activation on mechanoreflex modulation of carotid‐cardiac Gmax is unknown. Mechanoreflex stimulation by a standard passive calf stretch was performed during local circulatory occlusion in the resting limb, and after isometric calf contraction for 90s at 10, 30, 50 and 70% of maximum voluntary contraction (MVC). Heart rate and blood pressure were measured continuously. Throughout the protocol, pulsatile neck pressure trains (+40 to ‐80 Torr) were applied to derive carotid cardiac and vasomotor baroreflex function curves. As expected, there was a graded increase in blood pressure with graded metaboreflex activation. Gmax of the carotid‐cardiac baroreflex function curve was similarly reduced from rest during stretch in the 30, 50 and 70 % trials, by ‐50±7, ‐44±2 and ‐51±16 % respectively (P&lt;0.05). No significant reduction from rest was detected during the 0 and 10% trials. Gmax of the carotid‐vasomotor baroreflex function curves was unaffected by stretch. The results suggest that afferent feedback due to passive stretch in combination with metabolites accumulated during exercise at 30% MVC and above is sufficient to alter carotid‐cardiac baroreflex gain.

Spontaneous baroreflex measures are unable to detect age‐related impairments in cardiac baroreflex function during dynamic exercise in humans

The dynamic relationship between 'spontaneous' fluctuations in arterial blood pressure (BP) and heart rate (HR) is increasingly being used to provide an estimate of resting cardiac baroreflex sensitivity. Given the ease of use and clinical utility, spontaneous methods are now also being used to examine cardiac baroreflex sensitivity in distinct subject groups during various laboratory stressors and tasks encountered during daily life, such as physical activity. However, the utility of such spontaneous measures to estimate cardiac baroreflex function during exercise remains unclear, particularly when comparing groups. Therefore, we tested the ability of spontaneous indices to detect age-related differences in cardiac baroreflex function during dynamic exercise. Beat-to-beat HR and BP were measured in eighteen healthy young subjects (24 +/- 1 years) and sixteen healthy middle-aged subjects (59 +/- 1 years) at rest and during steady-state leg cycling. Estimates of spontaneous cardiac baroreflex sensitivity using the sequence technique (G(SEQ)) and low-frequency transfer function gain (G(TF)) were compared with the operating point (G(OP)) and maximal gain (G(MAX)) of the full carotid-cardiac baroreflex function curve. At rest G(SEQ), G(TF), G(OP) and G(MAX) were all significantly lower in older subjects. During moderate-intensity steady-state exercise no differences were observed in G(SEQ) and G(TF) (older 0.26 +/- 0.03 beats min(-1) mmHg(-1) versus younger 0.32 +/- 0.04 beats min(-1) mmHg(-1); P > 0.05), whereas G(OP) and G(MAX) (older -0.21 +/- 0.02 beats min(-1) mmHg(-1) versus younger -0.39 +/- 0.03 beats min(-1) mmHg(-1); P < 0.05) remained lower in older subjects. These data indicate that spontaneous measures of cardiac baroreflex sensitivity alone provide limited information when comparing age-groups during exercise, which makes genuine differences in baroreflex function difficult to identify.

Can Spontaneous Indices of Cardiac-Baroreflex Sensitivity Detect Age-Related Differences in Baroreflex Function During Dynamic Exercise?

PURPOSE: The dynamic relationship between "spontaneous" fluctuations in blood pressure and heart rate are increasingly being used to provide an estimate of resting cardiac baroreflex sensitivity. Given the ease of use and clinical utility, spontaneous methods are now also being used to examine cardiac baroreflex sensitivity during various laboratory stressors and tasks encountered during daily life, such as physical activity. In this study, we examined the ability of such spontaneous indices to detect age-related differences in cardiac baroreflex function during dynamic exercise. METHODS: Beat-to-beat heart rate and blood pressure were measured in five young (23 ± 1 yrs) and five older (59 ± 1 yrs) healthy subjects at rest and during steady-state leg cycling at 50% heart rate reserve. Low frequency transfer function gain between changes in mean blood pressure and heart rate (0.07-0.2 Hz; GTF) were used as an estimate of spontaneous cardiac baroreflex sensitivity. In addition, five second pulses of neck pressure and neck suction (+40 to -80 Torr) were applied to determine full carotid-cardiac baroreflex stimulus-response curves and maximal gain (GMAXX) and operating point gain (GOP) were calculated. RESULTS: At rest GTF was significantly lower in older subjects, whereas during and immunohistochemistry. steady-state exercise no differences were observed (0.26 ± 0.03 older vs. 0.32 ± 0.04 younger bpm/mmHg; P>0.05). Similar to GTF, the GOP and GMAX of the carotid-cardiac baroreflex function curve were lower in older subjects at rest. During exercise GOP was similar in both groups due to a reduction in younger subjects. In contrast, GMAX was unchanged from rest, and therefore remained lower in older subjects (−0.20 ± 0.03 older vs. −0.36 ± 0.05 younger bpm/mmHg; P < 0.05). CONCLUSIONS: In summary, the GTF and GOP were similar during dynamic exercise in young and older subjects whereas the GMAX was lower in older subjects. These data indicate that estimates of spontaneous cardiac baroreflex sensitivity are unable to detect age-related differences in maximal cardiac baroreflex gain during dynamic exercise and are more closely related to the gain around the operating point of the baroreflex function curve.

Does the Intensity of Muscle Metaboreflex Activation Influence Carotid-Cardiac Baroreflex Control in Humans?

Does the Intensity of Muscle Metaboreflex Activation Influence Carotid-Cardiac Baroreflex Control in Humans?

Effect of muscle metaboreflex activation on carotid-cardiac baroreflex function in humans

Whether the activation of metabolically sensitive skeletal muscle afferents (i.e., muscle metaboreflex) influences cardiac baroreflex responsiveness remains incompletely understood. A potential explanation for contrasting findings of previous reports may be related to differences in the magnitude of muscle metaboreflex activation utilized. Therefore, the present study was designed to investigate the influence of graded intensities of muscle metaboreflex activation on cardiac baroreflex function. In eight healthy subjects (24 +/- 1 yr), the graded isolation of the muscle metaboreflex was achieved by post-exercise ischemia (PEI) following moderate- (PEI-M) and high- (PEI-H) intensity isometric handgrip performed at 35% and 45% maximum voluntary contraction, respectively. Beat-to-beat heart rate (HR) and blood pressure were measured continuously. Rapid pulse trains of neck pressure and neck suction (+40 to -80 Torr) were applied to derive carotid baroreflex stimulus-response curves. Mean blood pressure increased significantly from rest during PEI-M (+13 +/- 3 mmHg) and was further augmented during PEI-H (+26 +/- 4 mmHg), indicating graded metaboreflex activation. However, the operating point gain and maximal gain (-0.51 +/- 0.09, -0.48 +/- 0.13, and -0.49 +/- 0.12 beats.min(-1).mmHg(-1) for rest; PEI-M and PEI-H) of the carotid-cardiac baroreflex function curve were unchanged from rest during PEI-M and PEI-H (P > 0.05 vs. rest). Furthermore, the carotid-cardiac baroreflex function curve was progressively reset rightward from rest to PEI-M to PEI-H, with no upward resetting. These findings suggest that the muscle metaboreflex contributes to the resetting of the carotid baroreflex control of HR; however, it would appear not to influence carotid-cardiac baroreflex responsiveness in humans, even with high-intensity activation during PEI.

Exercise intensity influences cardiac baroreflex function at the onset of isometric exercise in humans

We sought to examine the influence of exercise intensity on carotid baroreflex (CBR) control of heart rate (HR) and mean arterial pressure (MAP) at the onset of exercise in humans. To accomplish this, eight subjects performed multiple 1-min bouts of isometric handgrip (HG) exercise at 15, 30, 45 and 60% maximal voluntary contraction (MVC), while breathing to a metronome set at eupneic frequency. Neck suction (NS) of -60 Torr was applied for 5 s at end expiration to stimulate the CBR at rest, at the onset of HG (<1 s), and after approximately 40 s of HG. Beat-to-beat measurements of HR and MAP were recorded throughout. Cardiac responses to NS at onset of 15% (-12 +/- 2 beats/min) and 30% (-10 +/- 2 beats/min) MVC HG were similar to rest (-10 +/- 1 beats/min). However, HR responses to NS were reduced at the onset of 45% and 60% MVC HG (-6 +/- 2 and -4 +/- 1 beats/min, respectively; P < 0.001). In contrast to HR, MAP responses to NS were not different from rest at exercise onset. Furthermore, both HR and MAP responses to NS applied at approximately 40s of HG were similar to rest. In summary, CBR control of HR was transiently blunted at the immediate onset of high-intensity HG, whereas MAP responses were preserved demonstrating differential baroreflex control of HR and blood pressure at exercise onset. Collectively, these results suggest that carotid-cardiac baroreflex control is dynamically modulated throughout isometric exercise in humans, whereas carotid baroreflex regulation of blood pressure is well-maintained.

Influence of age on cardiac baroreflex function during dynamic exercise in humans

We investigated the influence of aging on cardiac baroreflex function during dynamic exercise in seven young (22 +/- 1 yr) and eight older middle-aged (59 +/- 2 yr) healthy subjects. Carotid-cardiac baroreflex function was assessed at rest and during moderate-intensity steady-state cycling performed at 50% heart rate reserve (HRR). Five-second pulses of neck pressure and neck suction from +40 to -80 Torr were applied to determine the operating point gain (G(OP)) and maximal gain (G(MAX)) of the full carotid-cardiac baroreflex function curve and examine baroreflex resetting during exercise. At rest, mean arterial pressure (MAP) and heart rate were similar between the younger and older subjects. In contrast, the resting G(OP) and G(MAX) were significantly lower in the older subjects. The increase in MAP from rest to exercise was greater in the older subjects (Delta +20 +/- 2 older vs. Delta +6 +/- 3 younger mmHg; P < 0.001). However, the G(OP) was similar in both groups during exercise because of a reduction in the younger subjects. In contrast, G(MAX) was unchanged from rest and therefore remained lower in older subjects (-0.19 +/- 0.05 older vs. -0.42 +/- 0.05 younger beats.min(-1).mmHg(-1); 50% HRR; P < 0.001). Furthermore, exercise resulted in an upward and rightward resetting of the cardiac baroreflex function curve in both groups. Collectively, these findings suggest that the cardiac baroreflex function curve appropriately resets during exercise in older subjects but operates at a reduced G(MAX) primarily because of age-related reductions in carotid-cardiac control manifest at rest.

WISE‐2005: The relation between standing balance and orthostatic tolerance in women

Introduction Previous studies suggest a complex interaction between the human autonomic, visual, vestibular systems and orthostatic tolerance (OT). The vestibular system potentially affects the carotid-cardiac baroreflex which may alter OT. We hypothesize that orthostatic tolerance is related to standing balance. Methods 24 healthy women performed balance tests consisting of standing on one foot on a 10cm wide beam in the width of the beam with eyes open (SBO) and closed (SBC) for up to 30s. The subjects were divided into those who could finish (F-SBC) and those who could not finish (NF-SBC) the 30s of SBC-test. Orthostatic tolerance (OT) was measured during a tilt/graded lower body negative pressure test by measuring the total time (s) the subject could tolerate the stress before the onset of pre-syncopal symptoms. SBO and SBC times were compared using a (within group) Wilcoxon Matched pairs test. OT times for the F-SBC and NF-SBC were compared using the Mann-Whitney U-test. Results Balance times were significantly longer (p<0.05) in SBO (30±0 s) than SBC (24±9 s). Significantly longer OT times (p<0.05) can be observed for F-SBC (1066±50 s) than for NF-SBC (944±41 s). Conclusion Visual input is important for postural control and may compensate for a possible effect of lower orthostatic tolerance on standing balance. Several factors can influence balance ability and orthostatic tolerance therefore further studies of SBC and OT are needed to determine the importance of this relationship and the physiological pathways involved. Supported by NASA, ESA, and CNES and by NASA Grant NNJ04HF71G to A. Hargens.

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.

Effects of Sevoflurane Anesthesia on Carotid-Cardiac Baroreflex Responses in Humans

Sevoflurane depresses cardio-vagal baroreflex gain (ability of vagally mediated R-R interval response to arterial blood pressure change). We examined the effects of sevoflurane anesthesia on maximum buffering capacity of vagally mediated hemodynamic control (baroreflex range) by examining the entire stimulus-response baroreflex relation. Electrocardiogram and invasive arterial blood pressure were monitored in 11 healthy volunteers. Carotid-cardiac baroreflex responses were elicited by increasing neck chamber pressure (external pressure applied over the bilateral carotid sinuses) to 40 mm Hg for 5 heartbeats followed by decreasing chamber pressure by successive 15-mm Hg R-wave triggered decrements to -65 mm Hg during held expiration. R-R intervals were plotted as functions of preceding carotid distending pressure. Range, maximum gain, and operational point (relative position of the resting set point within the entire baroreflex response curve) were determined at conscious baseline, during 2% (end-tidal) sevoflurane anesthesia, without and with phenylephrine infusion to maintain conscious arterial blood pressure, and at 30, 60, 120, and 180 min after emergence from anesthesia. Sevoflurane anesthesia significantly depressed maximum gain (from 3.84 +/- 0.99 to 1.04 +/- 0.40 ms/mm Hg [mean +/- sd]; P < 0.001) and range (from 207 +/- 43 to 52 +/- 19 ms; P < 0.001) of the reflex relation, both of which recovered at 120 and 180 min after emergence. Phenylephrine infusion only partially restored these variables. The operational point was unchanged throughout the study. Our results indicate that maximum cardio-vagal compensatory response to buffer hemodynamic perturbation is depressed during sevoflurane anesthesia. Sevoflurane-induced hypotension, which produced vagal withdrawal, did not play an important role in depressing cardio-vagal reflex function.

Functional interaction between nucleus tractus solitarius NK and 5-HT receptors in the inhibition of baroreflex in rats

Previous data showed that in the nucleus tractus solitarius (NTS), 5-HT(3) receptors are critically involved in the inhibition of cardiac baroreceptor reflex response occurring during the defense reaction. Since stimulation of NTS NK(1) receptors has been found to inhibit the baroreflex bradycardia, we examined in this study whether this reflex response is inhibited during the defense reaction via an interaction between NK(1) and 5-HT(3) receptors. For this purpose, we analyzed in urethane-anaesthetized rats the effects of intra-NTS GR205171, a selective NK(1) receptor antagonist, on the baroreflex bradycardia inhibition observed either during the defense reaction triggered by electrical stimulation of the dorsal periaqueductal grey matter (dPAG) or after NTS 5-HT(3) receptor activation. Intra-NTS GR205171, reversed, in dose-dependent manner, the inhibitory effect of dPAG stimulation on baroreflex bradycardia. This reversion was of 49% when both sinus carotid and aortic baroreceptors were stimulated by phenylephrine, and of 84% when aortic depressor nerve was stimulated. Similarly, intra-NTS GR205171 reversed partially or almost totally the inhibitory effect of local microinjections of phenylbiguanide, a 5-HT(3) receptor agonist, on baroreflex bradycardia induced either by phenylephrine administration or aortic nerve stimulation, respectively. These results strongly suggest that NK(1) receptors contribute downstream to the 5-HT(3) receptor-mediated inhibition of the aortic but not carotid cardiac baroreflex response occurring during the defense reaction, therefore implying that baroreceptor afferent inputs may be differentially modulated depending on their origin. This differentiation may be useful for a better understanding of baroreflex dysfunction in disease-induced conditions.

Does the menstrual cycle influence the sensitivity of vagally mediated baroreflexes?

The menstrual cycle provokes several physiological changes that could influence autonomic regulatory mechanisms. We studied the carotid-cardiac baroreflex in ten healthy young women on four occasions over the course of their menstrual cycles (days 0-8, 9-14, 15-20 and 21-25). We drew blood during each session for analysis of oestrogen, progesterone and noradrenaline (norepinephrine) levels, and assessed carotid-cardiac baroreflex function by analysing R-R interval responses to graded neck pressure sequences. Oestrogen levels followed a classical two-peak (cubic) response, with elevated levels on days 9-14 and 21-25 compared with days 0-8 and 15-20 (P=0.0032), while progesterone levels increased exponentially from days 9-14 to days 21-25 (P=0.0063). Noradrenaline levels increased from an average of 137 pg/ml during the first three measurement periods to 199 pg/ml during days 21-25 (P=0.0456). Carotid-cardiac baroreflex gain and operational point were not statistically different at any of the time points during the menstrual cycle (P> or =0.18). These findings are consistent with the notion that beat-to-beat vagal-cardiac regulation does not change over the course of the normal menstrual cycle.

Does the menstrual cycle influence the sensitivity of vagally mediated baroreflexes?

The menstrual cycle provokes several physiological changes that could influence autonomic regulatory mechanisms. We studied the carotid-cardiac baroreflex in ten healthy young women on four occasions over the course of their menstrual cycles (days 0-8, 9-14, 15-20 and 21-25). We drew blood during each session for analysis of oestrogen, progesterone and noradrenaline (norepinephrine) levels, and assessed carotid-cardiac baroreflex function by analysing R-R interval responses to graded neck pressure sequences. Oestrogen levels followed a classical two-peak (cubic) response, with elevated levels on days 9-14 and 21-25 compared with days 0-8 and 15-20 (P =0.0032), while progesterone levels increased exponentially from days 9-14 to days 21-25 (P = 0.0063). Noradrenaline levels increased from an average of 137pg/ml during the first three measurement periods to 199pg/ml during days 21-25 (P = 0.0456). Carotid-cardiac baroreflex gain and operational point were not statistically different at any of the time points during the menstrual cycle (P⩾0.18). These findings are consistent with the notion that beat-to-beat vagal-cardiac regulation does not change over the course of the normal menstrual cycle.

Carotid sinus "irritability" rather than hypersensitivity: a new name for an old syndrome?

Carotid sinus hypersensitivity (CSH) is a well-described cause of syncope, resulting in bradycardia and/or hypotension in response to neck pressure. The authors hypothesized that (CSH) represents an inappropriate response of the baroreflex system to a nonphysiologic stimulus, rather than a truly hypersensitive carotid sinus (ie, excessive vagotonia and sympathoinhibition in response to arterial hypertension). To test their hypothesis, the authors used a neck chamber to deliver stepped, R-wave-triggered changes in transmural carotid sinus pressure, from +40 to -60 mm Hg, during a single held expiration. The authors studied 7 men (age 69 +/- 8y; mean age +/- SD) with carotid sinus syndrome and 10 age- and sex-matched controls. Seven repetitions of pressure changes were averaged, and the carotid sinus response described by changes in the R-R interval. There was no statistical difference in carotid-cardiac baroreflex gain (R-R interval/pressure change; mean gain +/- SD, 3.0 +/- 2.1 msec/mm Hg and 2.2 +/- 3.0 msec/mm Hg, respectively) or other markers of carotid baroreflex responses between the subjects and controls. These preliminary results suggest that (CSH) may not be a "hypersensitive" reflex, but rather an inappropriate response, or "irritability," of the baroreflex system to nonphysiologic deformation of the carotid sinus and/or surrounding tissues.