Chronic vagotomy induces nTS glial activation, reduced glutamatergic signaling, and blunted cardiorespiratory responses DOI Open Access
Gabrielle C. Hofmann

Published: Jan. 1, 2023

The brainstem nucleus tractus solitarii (nTS) is the first site of integration viscerosensory information provided by afferents vagus nerves. nTS critically contributes to cardiorespiratory function and displays remarkable neuroplasticity in response changes afferent input. Vagal form synapses with neurons that are closely associated astrocytes, forming tripartite synapse. We hypothesized reducing vagal input via chronic unilateral vagotomy would alter synapse nTS, resulting activity. In results Aim 1, we showed induced astrocyte reactivity microglial activation nTS. This corresponded a reduction augmented breaths (sighs) during hypoxia. 2, further investigated effects stimulating recording sympathetic responses. Blunted responses stimulation lead us hypothesize reactive astrocytes at may be contributing this through increased glutamate uptake. Instead found evidence reduced excitability vagotomized decreased postsynaptic NMDA receptor function, leading blunted neuronal upon stimulation. Together these demonstrate multiple occur following vagotomy, contribute reflex affect health disease.

Language: Английский

Heart brain axis in health and disease: role of innate and adaptive immunity DOI Creative Commons
Alba Simats, Hendrik B. Sager, Arthur Liesz

et al.

Cardiovascular Research, Journal Year: 2024, Volume and Issue: unknown

Published: Aug. 24, 2024

Abstract The importance of the brain–heart interaction has been increasingly recognized as a critical physiological axis that is altered in disease. In this review, we explore intricate relationship between central nervous system and cardiovascular health, focusing particularly on immunological mechanisms influence course both neurological diseases. While previous studies have established key role autonomic (ANS) linking brain heart, more recent expanded our understanding multifaceted inter-organ interactions. As such, circulating mediators include immune cells adaptive innate their secreted immunogenic factors come into focus along bidirectional communication. Hence, review briefly discuss contribution ANS then heart-to-brain brain-to-heart axes, illustrating how diseases affect cognitive functions pathologies lead to cardiac complications.

Language: Английский

Citations

6
Effect of neuromodulation for chronic pain on the autonomic nervous system: a systematic review DOI Creative Commons
Bart Billet, Lisa Goudman, Philippe Rigoard

et al.

BJA Open, Journal Year: 2024, Volume and Issue: 11, P. 100305 - 100305

Published: Sept. 1, 2024

In recent years, there has been a growing interest in the use of neuromodulation as an alternative treatment option for chronic pain. Neuromodulation techniques, such spinal cord stimulation (SCS), dorsal root ganglion (DRG) stimulation, deep brain (DBS), and peripheral nerve have shown promising results management various pain conditions involve targeted modulation neural activity to alleviate restore functional capacity. The autonomic nervous system (ANS) plays crucial role regulation bodily functions including perception. However, effects on ANS context remain poorly understood. This systematic review aimed comprehensively assess existing literature about settings.

Language: Английский

Citations

3
Vagal nerve stimulation in myocardial ischemia/reperfusion injury: from bench to bedside DOI Creative Commons
Giuseppe Giannino,

Lorenzo Nocera,

Maria Andolfatto

et al.

Bioelectronic Medicine, Journal Year: 2024, Volume and Issue: 10(1)

Published: Sept. 13, 2024

Abstract The identification of acute cardioprotective strategies against myocardial ischemia/reperfusion (I/R) injury that can be applied in the catheterization room is currently an unmet clinical need and several interventions evaluated past at pre-clinical level have failed translation. Autonomic imbalance, sustained by abnormal afferent signalling, a key component I/R injury. Accordingly, there strong rationale for neuromodulation strategies, aimed reducing sympathetic activity and/or increasing vagal tone, this setting. In review we focus on cervical nerve stimulation (cVNS) transcutaneous auricular vagus (taVNS); latest has potential to overcome issues invasive cVNS, including possibility being used setting, while retaining its beneficial effects. First, discuss pathophysiology injury, mostly consequence overproduction reactive oxygen species. Second, describe functional anatomy parasympathetic branch autonomic nervous system most relevant principles bioelectronic medicine electrical modulation, with particular taVNS. Then, provide detailed comprehensive summary studies non-invasive VNS support effect whenever or chronic cardiac specifically setting benefit emerging field post arrest syndrome (PCAS) also mentioned. Indeed, cVNS anti-adrenergic, anti-inflammatory, antioxidants, anti-apoptotic pro-angiogenic effect; involved molecular pathways were already directly confirmed take place Pre-clinical data clearly show sooner applied, better outcome, marked infarct size reduction almost complete left ventricular reverse remodelling when immediately before during reperfusion. Finally, detail limited but very promising experience taVNS available so far.

Language: Английский

Citations

3
Cardiac parasympathetic denervation reduces hypoxic tachycardia, baroreflex sensitivity and heart rate variability in humans DOI Creative Commons
Piotr Niewiński, Stanisław Tubek, Krystian Josiak

et al.

Scientific Reports, Journal Year: 2025, Volume and Issue: 15(1)

Published: Feb. 24, 2025

The autonomic regulation of heart rate (HR) reactivity to acute hypoxia remains unclear. Parasympathetic cardioneuroablation (PCNA) may serve as a novel model for the analysis physiological consequences reduced vagal influence over sinus node in humans. We studied 11 adult patients scheduled PCNA treatment vasovagal syncope. HR was before and after with brief nitrogen gas administrations. Each test followed by an atropine challenge evaluate contribution parasympathetic tone resting HR. Additionally, we assessed changes cardiac baroreflex sensitivity variability following procedure. led partial denervation at rest (67.0 ± 20.1%). This translated into significant change (0.58 0.21 vs. 0.22 0.13 beats min− 1%SpO2 − 1, p = 0.0001) which proportional degree (R 0.76, 0.01). There no peak on implying unchanged sympathetic input node. suggests that is significantly influenced system. despite incomplete resulted profoundly depressed sensitivity. clinical meaning latter should be explored further studies.

Language: Английский

Citations

0
Cardiac output limits maximal oxygen consumption, but what limits maximal cardiac output? DOI Creative Commons
Ilkka Heinonen

Experimental Physiology, Journal Year: 2025, Volume and Issue: unknown

Published: April 7, 2025

Abstract Maximal oxygen uptake/consumption is an important variable determining exercise performance. It generally considered to be limited largely, but not exclusively, by maximal cardiac output (CO), which limits the ability of heart pump oxygen‐rich arterial blood working muscles. Cardiac a product rate and stroke volume, amount ejected from one beat. Exercise training, especially endurance type, can increase CO substantially. A straightforward way for would rate, this does happen; instead, tends reduced after training. This because most determinant myocardial consumption, ventricular filling flow (MBF) compromised further increases in given that MBF blunted contractions occurs principally during diastole. Myocardial extraction already high at rest increased endurance‐trained athletes, making their hearts even more dependent on MBF. The trained therefore also shows MBF, enhanced mean transit time higher vascular resistance submaximal exercise, although reserve improved. follows logically performance, it proposed review afferent sensory nerves might contribute controlling limiting hence CO, order protect ischaemia.

Language: Английский

Citations

0
From Physiology to Psychiatry: Key role of vagal interoceptive pathways in emotional control DOI
Jean‐Philippe Krieger, Karolina P. Skibicka

Biological Psychiatry, Journal Year: 2025, Volume and Issue: unknown

Published: April 1, 2025

Language: Английский

Citations

0
Myocardial infarction causes sex-dependent dysfunction in vagal sensory glutamatergic neurotransmission that is mitigated by 17β-Estradiol DOI Creative Commons

Asokan Devarajan,

Kerry Wang,

Zulfiqar A. Lokhandwala

et al.

JCI Insight, Journal Year: 2024, Volume and Issue: 9(14)

Published: June 17, 2024

Parasympathetic dysfunction after chronic myocardial infarction (MI) is known to predispose ventricular tachyarrhythmias (VT/VF). VT/VF MI more common in males than females. The mechanisms underlying the decreased vagal tone and associated sex difference occurrence of remain elusive. In this study, using optogenetic approaches, we found that responses glutamatergic afferent neurons were impaired following male mice, leading reduced reflex efferent parasympathetic function. Molecular analyses ganglia demonstrated glutamate levels, accompanied by mitochondrial function redox status infarcted vs. sham animals. Interestingly, females sensory impairment, with greater levels oxidative stress compared males. Treatment 17β-estradiol mitigated pathological remodeling improved neurotransmission mice. These data suggest a decrease results from signaling may be due homeostasis ganglia, which subsequently leads sex-dependent manner. Importantly, estrogen prevents improves MI.

Language: Английский

Citations

3
Cardiopulmonary nerve stimulation as a novel therapy for cardiac autonomic nervous system modulation DOI Creative Commons
Siamak Salavatian,

Julio Spinelli,

J. Schaefer

et al.

Frontiers in Neuroscience, Journal Year: 2024, Volume and Issue: 18

Published: Feb. 28, 2024

Cardiopulmonary nerve stimulation as a novel therapy for cardiac autonomic nervous system modulation

Language: Английский

Citations

2
Computational modelling of cardiac control following myocardial infarction using an in silico patient cohort DOI Creative Commons
Michelle Gee, Abraham M. Lenhoff, James S. Schwaber

et al.

The Journal of Physiology, Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 25, 2024

Abstract Loss of cardiac physiological function following myocardial infarction (MI) is accompanied by neural adaptations in the baroreflex that are compensatory short term, but then become associated with long‐term disease progression. One marker these decreased sensitivity, a strong predictor post‐MI mortality. The relative contributions remodelling and adaptation sensory, central brainstem peripheral ganglionic loci to sensitivity changes remain underexplored. We used computational model‐based approach accounts for short‐term dynamics closed‐loop human control integrate disparate experimental studies on MI into unified quantitative framework. developed an ensemble 59 distinct model parameterizations account clinically observed heterogeneity healthy individuals. simulated silico cohort 35,400 patients MI, corresponding six scenarios one or more coupled remodelling. evaluated range MI‐induced shifts arterial pressure, heart rate curve responses. Our results show any single locus sufficient haemodynamic autonomic experimentally. Of pathways, we found individuals vagal efferent preserved baroreceptor gain could maintain high after ischaemic injury. These suggest there multitude adaptive pathways tuning circuit shift physiology, potentially explaining patient post‐MI. image Key points Baroreflex indicator post‐myocardial ischaemia survival variable among fine‐tuned based observations develop consistent responses Simulation analysis functional afferent pathway ability adapt along can post‐cardiac ischaemia.

Language: Английский

Citations

2
Cardiac neurons expressing a glucagon-like receptor mediate cardiac arrhythmia induced by high-fat diet in Drosophila DOI Open Access
Yunpo Zhao, Jianli Duan, Joyce van de Leemput

et al.

Published: May 7, 2024

Cardiac arrhythmia leads to increased risks for stroke, heart failure, and cardiac arrest. Arrhythmic pathology is rooted in the conduction system, but mechanism complex not fully understood. For example, how metabolic diseases, like obesity diabetes, increase risk arrhythmia. Glucagon regulates glucose production, mobilizes lipids from fat body, affects rate rhythm, attributes of a likely key player. Drosophila an established model study diseases arrhythmias. Since glucagon signaling highly conserved, we used high-fat diet (HFD)-fed flies its effect on function. HFD led heartbeat irregular rhythm. The HFD-fed showed levels adipokinetic hormone (Akh), functional equivalent human glucagon. Both genetic reduction Akh eliminating producing cells (APC) rescued HFD-induced arrhythmia, whereas rhythm was normal receptor mutants ( AkhR null ). Furthermore, discovered pair neurons that express high receptor. These are located near posterior heart, make synaptic connections at muscle, regulate Altogether, this pathway provides new understanding regulatory mechanisms between disease

Language: Английский

Citations

1