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Neurological Sciences : Official... Jan 2021Initial cardiovascular fingolimod effects might compromise baroreflex responses to rapid blood pressure (BP) changes during common Valsalva-like maneuvers. This study...
BACKGROUND AND PURPOSE
Initial cardiovascular fingolimod effects might compromise baroreflex responses to rapid blood pressure (BP) changes during common Valsalva-like maneuvers. This study evaluated cardiovascular responses to Valsalva maneuver (VM)-induced baroreceptor unloading and loading upon fingolimod initiation.
PATIENTS AND METHODS
Twenty-one patients with relapsing-remitting multiple sclerosis performed VMs before and 0.5, 1, 2, 3, 4, 5, and 6 hours after fingolimod initiation. We recorded heart rate (HR) as RR intervals (RRI), systolic and diastolic BP (BPsys, BPdia) during VM phase 1, VM phase 2 early, VM phase 2 late, and VM phase 4. Using linear regression analysis between decreasing BPsys and RRI values during VM phase 2 early, we determined baroreflex gain (BRG) reflecting vagal withdrawal and sympathetic activation upon baroreceptor unloading. To assess cardiovagal activation upon baroreceptor loading, we calculated Valsalva ratios (VR) between maximal and minimal RRIs after strain release. Analysis of variance or Friedman tests with post hoc analysis compared corresponding parameters at the eight time points (significance: p < 0.05).
RESULTS
RRIs at VM phase 1, VM phase 2 early, and VM phase 2 late were higher after than before fingolimod initiation, and maximal after 4 hours. Fingolimod did not affect the longest RRIs upon strain release, but after 3, 5, and 6 hours lowered the highest BPsys values during overshoot and all BPdia values, and thus reduced VRs. BRG was slightly higher after 3 and 5 hours, and significantly higher after 4 hours than before fingolimod initiation.
CONCLUSIONS
VR-decreases 3-6 hours after fingolimod initiation are physiologic results of fingolimod-associated attenuations of BP and HR increases at the end of strain and do not suggest impaired cardiovagal activation upon baroreceptor loading. Stable and at the time of HR nadir significantly increased BRGs indicate improved responses to baroreceptor unloading. Thus, cardiovascular fingolimod effects do not impair autonomic responses to sudden baroreceptor loading or unloading but seem to be mitigated by baroreflex resetting.
Topics: Baroreflex; Blood Pressure; Fingolimod Hydrochloride; Heart Rate; Humans; Pressoreceptors; Valsalva Maneuver
PubMed: 33443674
DOI: 10.1007/s10072-020-05004-1 -
Journal of the American Society of... Jun 2019
Review
Topics: Animals; Humans; Ion Channels; Mechanotransduction, Cellular; Mice; Pressoreceptors; Sensitivity and Specificity
PubMed: 31043433
DOI: 10.1681/ASN.2019020160 -
Cell Reports Nov 2019Soohong et al. (2019) reveal a class of vagal afferents-defined by Piezo2 expression-that innervate the aorta and function to sense blood pressure fluctuations. Their...
Soohong et al. (2019) reveal a class of vagal afferents-defined by Piezo2 expression-that innervate the aorta and function to sense blood pressure fluctuations. Their study describes the morphologies and role of these neurons in vascular regulation.
Topics: Animals; Aorta; Baroreflex; Blood Pressure; Hoof and Claw; Pressoreceptors
PubMed: 31747586
DOI: 10.1016/j.celrep.2019.11.031 -
Kidney360 Dec 2022Heart failure is the most common cardiovascular complication of chronic kidney disease (CKD) and foreshadows a high morbidity and mortality rate. Baroreflex impairment...
BACKGROUND
Heart failure is the most common cardiovascular complication of chronic kidney disease (CKD) and foreshadows a high morbidity and mortality rate. Baroreflex impairment likely contributes to cardiovascular mortality. We aimed to study the associations between CKD, heart failure, and baroreflex sensitivity (BRS) and their association with cardiovascular outcomes.
METHODS
We retrospectively analyzed data from a cohort of 247 individuals with moderate to severe HF. All subjects underwent BRS measurements after intravenous phenylephrine along with electrocardiography, echocardiography, and laboratory measurements. We used logistic regression models to assess the association of CKD (estimated glomerular filtration rate <60 ml/min per 1.73 m) with BRS using iterative models. Cox proportional hazards models were used to assess associations of binary BRS and subgroups according to categorizations of CKD and BRS with cardiovascular mortality.
RESULTS
Median eGFR among individuals with CKD was 52 (IQR 44-56) ml/min per 1.73 m. eGFR was lower in those with depressed BRS (65 [IQR 54-76] ml/min per 1.73 m) compared with those with preserved BRS (73 [IQR 64-87] ml/min per 1.73 m; ≤0.001). The majority of individuals with CKD had depressed BRS compared with those without CKD (60% versus 29%; =0.05). In regression models, CKD and BRS were independently associated. Cardiovascular mortality was significantly increased in individuals with or without CKD and depressed BRS compared with those with preserved BRS and CKD.
CONCLUSIONS
Cardiac BRS is depressed in patients with mild to moderate CKD and HF and associated with cardiovascular mortality. Additional study to confirm its contribution to cardiovascular mortality, particularly in advanced CKD, is warranted.
Topics: Humans; Pressoreceptors; Retrospective Studies; Heart Failure; Kidney; Renal Insufficiency, Chronic
PubMed: 36591344
DOI: 10.34067/KID.0004812022 -
Pflugers Archiv : European Journal of... Aug 2023Reflex summation in the expression of left and right aortic baroreflex control of hemodynamic functions was investigated. In anesthetized Sprague-Dawley rats, mean...
Reflex summation in the expression of left and right aortic baroreflex control of hemodynamic functions was investigated. In anesthetized Sprague-Dawley rats, mean arterial pressure (MAP), heart rate (HR), and mesenteric vascular resistance (MVR) were recorded following left, right, and bilateral stimulation of the aortic depressor nerve (ADN). Stimulation frequency was varied between low (1 Hz), moderate (5 Hz), and high (20 Hz). At 1 Hz, left and right ADN stimulation evoked similar depressor, bradycardic and MVR responses, whereas bilateral stimulation induced larger MAP, HR, and MVR reductions compared with stimulations of either side. The sum of the separate and combined stimulation effects on MAP, HR, and MVR was similar, indicating an additive summation. A similar additive summation was observed with HR responses at 5 and 20 Hz. Left-sided and bilateral stimulation produced greater depressor and MVR responses than right-sided stimulation, with responses of the bilateral stimulation mimicking those of the left side. The bilateral MAP or MVR response was smaller than the sum of the separate responses, suggesting an inhibitory summation. In conclusion, reflex summation of the left and right aortic baroreceptor afferent input is differentially expressed in relation to the frequency of the input signal. Summation of baroreflex control of HR is always additive and independent of stimulation frequency. Summation of baroreflex control of MAP is additive when the frequency input is small and inhibitory when the frequency input is moderate to high, with MAP changes mainly driven by parallel baroreflex-triggered changes in vascular resistance.
Topics: Rats; Animals; Pressoreceptors; Rats, Sprague-Dawley; Blood Pressure; Electric Stimulation; Reflex; Baroreflex; Heart Rate
PubMed: 37219603
DOI: 10.1007/s00424-023-02820-0 -
Expert Review of Cardiovascular Therapy 2015With respect to paired internal organs, we commonly think that these are symmetrical and have identical physiological functions. This, however, appears not to be the...
With respect to paired internal organs, we commonly think that these are symmetrical and have identical physiological functions. This, however, appears not to be the case. A particular organ where asymmetry comes to expression is the baroreceptor system. Clinical data in patients with resistant hypertension who are treated with device-based baroreceptor activation clearly show that there are functional differences between the left and the right baroreceptor systems. This has implications for our understanding of certain diseases.
Topics: Blood Pressure; Humans; Hypertension; Pressoreceptors
PubMed: 26106932
DOI: 10.1586/14779072.2015.1049533 -
International Journal of... Oct 2018Concussion is defined as a complex pathophysiological process affecting the brain that is induced by the application or transmission of traumatic biomechanical forces to... (Review)
Review
Concussion is defined as a complex pathophysiological process affecting the brain that is induced by the application or transmission of traumatic biomechanical forces to the head. The result of the impact is the onset of transient symptoms that may be experienced for approximately 2weeks in most individuals. However, in some individuals, symptoms may not resolve and persist for a protracted period and a chronic injury ensues. Concussion symptoms are generally characterized by their emergence through changes in affect, cognition, or multi-sensory processes including the visual and vestibular systems. An emerging consequence of concussion is the presence of cardiovascular autonomic nervous system dysfunction that is most apparent through hemodynamic perturbations and provocations. Further interrogation of data that are derived from continuous digital electrocardiograms and/or beat-to-beat blood pressure monitoring often reveal an imbalance of parasympathetic or sympathetic nervous system activity during a provocation after an injury. The disturbance is often greatest early after injury and a resolution of the dysfunction occurs in parallel with other symptoms. The possibility exists that the disturbance may remain if the concussion does not resolve. Unfortunately, there is little evidence in humans to support the etiology for the emergence of this post-injury dysfunction. As such, evidence from experimental models of traumatic brain injury and casual observations from human studies of concussion implicate a transient abnormality of the anatomical structures and functions of the cardiovascular autonomic nervous system. The purpose of this review article is to provide a mechanistic narrative of multi-disciplinary evidence to support the anatomical and physiological basis of cardiovascular autonomic nervous system dysfunction after concussion. The review article will identify the anatomical structures of the autonomic nervous system and propose a theoretical framework to demonstrate the potential effects of concussive head trauma on corresponding outcome measurements. Evidence from experimental models will be used to describe abnormal cellular functions and provide a hypothetical mechanistic basis for the respective responses of the anatomical structures to concussive head trauma. When available, example observations from the human concussion literature will be presented to demonstrate the effects of concussive head trauma that may be related to anomalous activity in the respective anatomical structures of the autonomic nervous system.
Topics: Athletic Injuries; Baroreflex; Blood Pressure; Brain Concussion; Cerebral Cortex; Humans; Parasympathetic Nervous System; Pressoreceptors; Sympathetic Nervous System
PubMed: 29197614
DOI: 10.1016/j.ijpsycho.2017.11.016 -
Circulation. Arrhythmia and... Apr 2021Symptomatic heart failure (HF) patients despite optimal medical therapy and advances such as invasive hemodynamic monitoring remain challenging to manage. While cardiac... (Review)
Review
Symptomatic heart failure (HF) patients despite optimal medical therapy and advances such as invasive hemodynamic monitoring remain challenging to manage. While cardiac resynchronization therapy remains a highly effective therapy for a subset of HF patients with wide QRS, a majority of symptomatic HF patients are poor candidates for such. Recently, cardiac contractility modulation, neuromodulation based on carotid baroreceptor stimulation, and phrenic nerve stimulation have been approved by the US Food and Drug Administration and are emerging as therapeutic options for symptomatic HF patients. This state-of-the-art review examines the role of these evolving electrical therapies in advanced HF.
Topics: Animals; Autonomic Nervous System; Cardiac Pacing, Artificial; Electric Stimulation Therapy; Heart; Heart Failure; Humans; Myocardial Contraction; Pacemaker, Artificial; Prevalence; Recovery of Function; Spinal Cord Stimulation; Stroke Volume; Treatment Outcome; Vagus Nerve Stimulation; Ventricular Function, Left
PubMed: 33858178
DOI: 10.1161/CIRCEP.120.009668 -
Obesity (Silver Spring, Md.) Jun 2023Sympathetic nervous system overactivation and abnormal lipid metabolism are featured in obesity and may lead to cardiac remodeling. The effects of carotid baroreceptor...
OBJECTIVE
Sympathetic nervous system overactivation and abnormal lipid metabolism are featured in obesity and may lead to cardiac remodeling. The effects of carotid baroreceptor stimulation (CBS) on cardiac remodeling in obese rats and the underlying mechanisms were explored.
METHODS
An obesity model was induced by 16-week high-fat diet feeding. A CBS device was implanted at the 8th week. Body weight and blood pressure measurements, electrocardiography, echocardiography, and glucose and insulin tolerance tests were conducted before sampling. Plasma analysis and histological and biological analyses of left ventricle were also performed. Neonatal rat cardiomyocytes cocultured with 3T3-L1 in transwell chambers were used to investigate the mechanisms.
RESULTS
CBS alleviated several manifestations of obesity, including increased body weight, high blood pressure, hyperlipidemia, and enhanced sympathetic activity. In obese hearts, norepinephrine levels decreased, and the monoamine oxidase A (MAO-A) and reactive oxygen species level increased; these changes, as well as cardiac fibrosis, lipid metabolic disorders, and heart dysfunction, were inhibited by CBS. Neonatal rat cardiomyocytes incubated with norepinephrine showed MAO-A upregulation, increased reactive oxygen species levels, lipid metabolic disorders, and inflammatory response, which were inhibited by clorgyline, a selective MAO-A inhibitor.
CONCLUSIONS
CBS effectively suppresses sympathetic nervous system activity and oxidative stress mediated by MAO-A and prevents cardiac remodeling in obese rats.
Topics: Rats; Animals; Monoamine Oxidase; Pressoreceptors; Reactive Oxygen Species; Ventricular Remodeling; Oxidative Stress; Obesity; Lipids; Norepinephrine
PubMed: 36998154
DOI: 10.1002/oby.23729 -
Circulation Dec 2015
Topics: Baroreflex; Female; Heart-Assist Devices; Hemodynamics; Humans; Male; Pressoreceptors; Pulsatile Flow; Ventricular Function, Left
PubMed: 26510697
DOI: 10.1161/CIRCULATIONAHA.115.019461