Surgical aortic valve replacement (SAVR) and transcatheter aortic valve implantation (TAVI) are options in severe aortic valve stenosis (AVS). Cardiovascular (CV) and cerebrovascular (CBV) control markers, derived from variability of heart period, systolic arterial pressure, mean cerebral blood velocity and mean arterial pressure, were acquired in 19 AVS patients (age: 76.8 ± 3.1 yrs, eight males) scheduled for SAVR and in 19 AVS patients (age: 79.9 + 6.5 yrs, 11 males) scheduled for TAVI before (PRE) and after intervention (POST, <7 days). Left ventricular function was preserved in both groups. Patients were studied at supine resting (REST) and during active standing (STAND). We found that: (i) both SAVR and TAVI groups featured a weak pre-procedure CV control; (ii) TAVI ensured better CV control; (iii) cerebral autoregulation was working in PRE in both SAVR and TAVI groups; (iv) SAVR and TAVI had no impact on the CBV control; (v) regardless of group, CV and CBV control markers were not influenced by STAND in POST. Even though the post-procedure preservation of both CV and CBV controls in TAVI group might lead to privilege this procedure in patients at higher risk, the missing response to STAND suggests that this advantage could be insignificant.

Protection of cranial nerves is one of the major challenges in the resection of paragangliomas of head and neck, especially in complex paragangliomas. We report a case of bilateral jugular tumor with unilateral carotid body tumor. Baroreflex failure syndrome（BFS） occurred after staged resection of bilateral lesions. There is still a lack of effective treatment for this complication. More prudent and reasonable treatment strategy is important to reduce the incidence of BFS.
摘要：颅神经保护是头颈部副神经节瘤（Paragangliomas）切除术的主要挑战之一，特别是对于同时发生在双侧的复杂副神经节瘤病例。本文报道了1例双侧颈静脉球瘤合并单侧颈动脉体瘤的病例，在分期切除双侧病灶后发生了压力反射衰竭综合征。这种并发症尚缺乏有效的治疗手段，制定谨慎而合理的治疗策略是降低其发生率的关键。.

BACKGROUND: Chronic kidney disease (CKD) is characterized by over-activation of the sympathetic nervous system (SNS) that increases cardiovascular risk. Whether sympathetic baroreflex sensitivity (sBRS) is impaired or intact in CKD remains under-studied and controversial. Furthermore, the downstream effect of SNS activation on blood pressure transduction has not been previously examined in CKD. We tested the hypothesis that sBRS is attenuated, while sympathetic transduction is augmented in CKD.
METHODS: In 18 sedentary patients with CKD stages III-IV (eGFR: 40±14 ml/min) and 13 age-matched controls (eGFR: 95±10 ml/min), beat-to-beat blood pressure (BP; finger photoplethysmography), heart rate (electrocardiography) and muscle sympathetic nerve activity (MSNA; microneurography) were recorded at rest for 10-min. Weighted linear regression analysis between MSNA burst incidence and diastolic BP was used to determine the spontaneous sBRS. Sympathetic-BP transduction was quantified using signal averaging, whereby the BP response to each MSNA burst was tracked over 15 cardiac cycles and averaged to derive the peak change in BP.
RESULTS: Compared with controls, CKD patients had an attenuated sBRS [CKD: -1.34±0.59 versus CON: -2.91±1.09 bursts (100 heartbeats)-1 mmHg-1; P=0.001]. |sBRS| was significantly associated with eGFR (r=0.69, P<0.001). CKD patients had attenuated sympathetic-BP transduction compared to controls (0.75±0.7 vs. 1.60±0.8 mmHg; P=0.010). Resting MSNA was negatively associated with sympathetic transduction (r=-0.57, P=0.002).
CONCLUSIONS: CKD patients exhibit impaired sBRS that may contribute to SNS overactivation and cardiovascular risk in this patient population. In addition, CKD patients had an attenuated sympathetic transduction that may counteract the vascular effects of SNS overactivation.

Social pain is a painful feeling evoked by social rejection, exclusion, or the loss of other important people. Previous research suggests that physical pain is reduced by increased signals from baroreceptors that monitor blood pressure. This pre-registered study investigated whether social pain is attenuated by increased baroafferent signals, as observed in physical pain. Given that baroafferent signals increase during cardiac systole and decrease during diastole, we hypothesized that feelings of pain induced by social rejection would be lower when exclusion events are presented at the cardiac systole than when they are presented at the diastole. Participants completed the cyberball task, a computerized ball-tossing game involving two other players. In the rejection condition, the ball was rarely thrown to the participant, while the other players kept tossing it to each other. Throws between other players were defined as exclusion events and were presented either at the cardiac systole (a systole condition) or at the diastole (a diastole condition). We found that exclusion events evoked significantly less social pain in the systole condition than in the diastole condition. Furthermore, the effects of cardiac cycle were more pronounced in participants with higher heart rate variability than those with lower heart rate variability. Our results suggest that cardiac afferent signals contribute not only to physical pain but also to social pain.

Under simultaneous ambient temperature and postural stressors, integrated regional blood flow responses are required to maintain blood pressure and thermoregulatory homeostasis. The aim of the present study was to assess the effect of ambient temperature and body posture on regional regulation of microvascular blood flow, specifically in the arms and legs. Participants (N = 11) attended two sessions in which they experienced transient ambient conditions, in a climatic chamber. During each 60-min trial, ambient temperature increased from 15.7 (0.6) °C to 38.9 (0.6) °C followed by a linear decrease, and the participants were either standing or in a supine position throughout the trial; relative humidity in the chamber was maintained at 25.9 (6.6) %. Laser doppler flowmetry of the forearm (SkBFarm) and calf (SkBFcalf), and haemodynamic responses (heart rate, HR; stroke volume, SV; cardiac output, CO; blood pressure, BP), were measured continuously. Analyses of heart rate variability and wavelet transform were also conducted. SkBFarm increased significantly at higher ambient temperatures (p = 0.003), but not SkBFcalf. The standing posture caused lower overall SkBF in both regions throughout the protocol, regardless of temperature (p < 0.001). HR and BP were significantly elevated, and SV significantly lowered, in response to separate and combined effects of higher ambient temperatures and a standing position (all p < 0.05); CO remained unchanged. Mechanistic analyses identified greater sympathetic nerve activation, and higher calf myogenic activation at peak temperatures, in the standing condition. Mechanistically and functionally, arm vasculature responds to modulation from both thermoregulation and baroreceptor activity. The legs, meanwhile, are more sensitive to baroreflex regulatory mechanisms.

Preclinical models indicate that amiloride (AMD) reduces baroreflex sensitivity and perturbs homeostatic blood pressure (BP) regulation. However, it remains unclear whether these findings translate to humans. This study investigated whether oral administration of AMD reduces spontaneous cardiac and sympathetic baroreflex sensitivity and perturbs BP regulation in healthy young humans. Heart rate (HR; electrocardiography), beat-to-beat BP (photoplethysmography), and muscle sympathetic activity (MSNA, microneurography) were continuously measured in 10 young subjects (4 females) during rest across two randomized experimental visits: 1) after 3 h of oral administration of placebo (PLA, 10 mg of methylcellulose within a gelatin capsule) and 2) after 3 h of oral administration of AMD (10 mg). Visits were separated for at least 48 h. We calculated the standard deviation and other indices of BP variability. Spontaneous cardiac baroreflex was assessed via the sequence technique and cardiac autonomic modulation through time- and frequency-domain HR variability. The sensitivity (gain) of the sympathetic baroreflex was determined via weighted linear regression analysis between MSNA and diastolic BP. AMD did not affect HR, BP, and MSNA compared with PLA. Indexes of cardiac autonomic modulation (time- and frequency-domain HR variability) and BP variability were also unchanged after AMD ingestion. Likewise, AMD did not modify the gain of both spontaneous cardiac and sympathetic arterial baroreflex. A single oral dose of AMD does not affect spontaneous arterial baroreflex sensitivity and BP variability in healthy young adults.NEW & NOTEWORTHY Preclinical models indicate that amiloride (AMD), a nonselective antagonist of the acid-sensing ion channels (ASICs), impairs baroreflex sensitivity and perturbs blood pressure regulation. We translated these findings into humans, investigating the impact of acute oral ingestion of AMD on blood pressure variability and spontaneous cardiac and sympathetic baroreflex sensitivity in healthy young humans. In contrast to preclinical evidence, AMD does not impair spontaneous arterial baroreflex sensitivity and blood pressure variability in healthy young adults.

OBJECTIVE: Hypertension is one of the major causes of cardiovascular morbidity and mortality in the USA and disproportionately affects Black women. Endothelial-derived nitric oxide (eNO) substantially regulates blood pressure in humans, and impaired NO-mediated vasodilation has been reported in the Black population. Previous studies using an NO synthase inhibitor, NG-monomethyl-L-arginine (L-NMMA) did not fully determine the NO contribution to blood pressure because of baroreflex buffering. Therefore, in the present study we used trimethaphan, a ganglionic blocker, to inhibit baroreflex buffering and study NO modulation of blood pressure in Black women during L-NMMA infusion.
METHODS: L-NMMA at doses of 250 μg/kg per minute was infused in combination with trimethaphan at doses of 4 mg/min to eliminate baroreflex mechanisms. Heart rate (HR) was obtained with continuous electrocardiogram monitoring, and continuous blood pressure was measured with the volume clamp method. The increase in systolic blood pressure (SBP) during both infusions was used to estimate the contribution of NO to blood pressure.
RESULTS: Ten Black (age range 30-50 years, body mass index [BMI] 30-45 kg/m2), and nine White women (age range 30-50 years, body mass index 30-45 kg/m2) were enrolled in this study. During autonomic blockade, there was no difference in the decrease in SBP between Black and White women (- 20 ± 16.45 vs. - 24 ± 15.49 mm Hg, respectively; P = 0.659). When autonomic blockade was combined with L-NMMA, Black women had a significant increase in SBP compared to White women (54 ± 13.62 vs. 39 ± 09.64 mm Hg, respectively; P = 0.022, respectively).
CONCLUSIONS: Autonomic blood pressure regulation was similar between Black and White women. However, NO contribution to blood pressure was significantly greater in Black women compared to White women.
BACKGROUND: ClinicalTrials.gov: NCT01122407.

Aortic baroreceptor afferents act as targets for blood pressure control in hypertension.

Permanent residence at high-altitude and chronic mountain sickness (CMS) may alter the cerebrovascular homeostasis and orthostatic responses. Healthy male participants living at sea-level (LL; n = 15), 3800 m (HL3800m; n = 13) and 5100 m (HL5100m; n = 17), respectively, and CMS highlanders living at 5100 m (n = 31) were recruited. Middle cerebral artery mean blood flow velocity (MCAv), cerebral oxygen delivery (CDO2), mean blood pressure (MAP), heart rate variability and spontaneuous cardiac baroreflex sensitivity (cBRS) were assessed while sitting, initial 30 s and after 3 min of standing. Cerebral autoregulation index (ARI) was estimated (ΔMCAv%baseline)/ΔMAP%baseline) in response to the orthostatic challenge. Altitude and CMS were associated with hypoxemia and elevated hemoglobin concentration. While sitting, MCAv and LFpower negatively correlated with altitude but were not affected by CMS. CDO2 remained preserved. BRS was comparable across all altitudes, but lower with CMS. Within initial 30 s of standing, altitude and CMS correlated with a lesser ΔMAP while ARI remained unaffected. After 3 min standing, MCAv, CDO2 and cBRS remained preserved across altitudes. The LF/HF ratio increased in HL5100m compared to LL and HL3800m from sitting to standing. In contrary, CMS showed blunted autonomic nervous activation in responses to standing. Despite altitude- and CMS-associated hypoxemia, erythrocytosis and impaired blood pressure regulation (CMS only), cerebral homeostasis remained overall preserved.

In this work, we couple a lumped-parameter closed-loop model of the cardiovascular system with a physiologically-detailed mathematical description of the baroreflex afferent pathway. The model features a classical Hodgkin-Huxley current-type model for the baroreflex afferent limb (primary neuron) and for the second-order neuron in the central nervous system. The pulsatile arterial wall distension triggers a frequency-modulated sequence of action potentials at the afferent neuron. This signal is then integrated at the brainstem neuron model. The efferent limb, representing the sympathetic and parasympathetic nervous system, is described as a transfer function acting on heart and blood vessel model parameters in order to control arterial pressure. Three in silico experiments are shown here: a step increase in the aortic pressure to evaluate the functionality of the reflex arch, a hemorrhagic episode and an infusion simulation. Through this model, it is possible to study the biophysical dynamics of the ionic currents proposed for the afferent limb components of the baroreflex during the cardiac cycle, and the way in which currents dynamics affect the cardiovascular function. Moreover, this system can be further developed to study in detail each baroreflex loop component, helping to unveil the mechanisms involved in the cardiovascular afferent information processing.