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Current Cardiology Reviews 2021The heart is the central organ of the circulatory system, which maintains the flow of blood along with the transport of nutrients to different cells and tissues. A... (Review)
Review
BACKGROUND
The heart is the central organ of the circulatory system, which maintains the flow of blood along with the transport of nutrients to different cells and tissues. A well-functioning cardiac state is a complicated mode of changeability. A healthy heart is not only about oscillation, as the rhythmometer is not the same in every circumstance. Heart rate shows variations so that it can be regulated according to psychophysiological conditions to maintain the effect of the internal-external stimulus.
OBJECTIVE
The main objective of this review is to provide a piece of all-inclusive information about heart rate variability (HRV) and different variables affecting HRV. The direct interconnection so that HRV can be used in clinical practices.
METHODS
This review article contains a detailed survey of literature about HRV available in different online sources such as; Google Scholar, Science Direct, PubMed, and Web of Science, etc. In this review, the authors have focused on the role of the autonomic nervous system in the regulation of HRV and the role of various factors affecting HRV.
RESULTS
The variation in the time between two heartbeats is termed as HRV. It is one of the indicators of many pathological conditions related to cardiovascular health. It provided reliable information about the interaction of the sympathetic and parasympathetic nervous systems. The analysis of the variation of heart rate is a well-known non-invasive technique to identify the functioning of the autonomic nervous system. The autonomic nervous system (ANS) depends on the sympathetic and parasympathetic nervous system for transferring information. The cardio-accelerating center, lungs, and non-striated muscles are innervated by cardiac sympathetic nerves. This division of ANS latches upon the heart accordingly via the cervicothoracic ganglion and vagus nerve. It is found that cardiac normal variability depends upon this stimulation towards the sinoatrial node (pacemaker), which can be evaluated by analyzing the HRV. In human-based studies, it has been found that a low level of HRV is one of the main causes of death rate among adults. Hence, HRV helps in identifying the risk of cardiac diseases and the state of ANS.
CONCLUSION
The heart plays a vital role in the human body and the well-functioning of the cardiac system is the need for a healthy life. The heart contains its nervous system termed as neurocardio system in which ANS plays a key role in which the sympathetic and parasympathetic systems interplay to regulate HRV. High HRV is associated with healthy condition, while low HRV is associated with pathological conditions. The HRV is influenced by various variables such as; pathological, physiological, psychological, environmental factors, lifestyle factors, and genetic factors, etc.
Topics: Autonomic Nervous System; Heart; Heart Rate; Humans
PubMed: 33390146
DOI: 10.2174/1573403X16999201231203854 -
Nature May 2022Atherosclerotic plaques develop in the inner intimal layer of arteries and can cause heart attacks and strokes. As plaques lack innervation, the effects of neuronal...
Atherosclerotic plaques develop in the inner intimal layer of arteries and can cause heart attacks and strokes. As plaques lack innervation, the effects of neuronal control on atherosclerosis remain unclear. However, the immune system responds to plaques by forming leukocyte infiltrates in the outer connective tissue coat of arteries (the adventitia). Here, because the peripheral nervous system uses the adventitia as its principal conduit to reach distant targets, we postulated that the peripheral nervous system may directly interact with diseased arteries. Unexpectedly, widespread neuroimmune cardiovascular interfaces (NICIs) arose in mouse and human atherosclerosis-diseased adventitia segments showed expanded axon networks, including growth cones at axon endings near immune cells and media smooth muscle cells. Mouse NICIs established a structural artery-brain circuit (ABC): abdominal adventitia nociceptive afferents entered the central nervous system through spinal cord T-T dorsal root ganglia and were traced to higher brain regions, including the parabrachial and central amygdala neurons; and sympathetic efferent neurons projected from medullary and hypothalamic neurons to the adventitia through spinal intermediolateral neurons and both coeliac and sympathetic chain ganglia. Moreover, ABC peripheral nervous system components were activated: splenic sympathetic and coeliac vagus nerve activities increased in parallel to disease progression, whereas coeliac ganglionectomy led to the disintegration of adventitial NICIs, reduced disease progression and enhanced plaque stability. Thus, the peripheral nervous system uses NICIs to assemble a structural ABC, and therapeutic intervention in the ABC attenuates atherosclerosis.
Topics: Animals; Atherosclerosis; Disease Progression; Ganglia, Spinal; Ganglia, Sympathetic; Mice; Neurons; Plaque, Atherosclerotic
PubMed: 35477759
DOI: 10.1038/s41586-022-04673-6 -
Nature Jul 2020Connections between the gut and brain monitor the intestinal tissue and its microbial and dietary content, regulating both physiological intestinal functions such as...
Connections between the gut and brain monitor the intestinal tissue and its microbial and dietary content, regulating both physiological intestinal functions such as nutrient absorption and motility, and brain-wired feeding behaviour. It is therefore plausible that circuits exist to detect gut microorganisms and relay this information to areas of the central nervous system that, in turn, regulate gut physiology. Here we characterize the influence of the microbiota on enteric-associated neurons by combining gnotobiotic mouse models with transcriptomics, circuit-tracing methods and functional manipulations. We find that the gut microbiome modulates gut-extrinsic sympathetic neurons: microbiota depletion leads to increased expression of the neuronal transcription factor cFos, and colonization of germ-free mice with bacteria that produce short-chain fatty acids suppresses cFos expression in the gut sympathetic ganglia. Chemogenetic manipulations, translational profiling and anterograde tracing identify a subset of distal intestine-projecting vagal neurons that are positioned to have an afferent role in microbiota-mediated modulation of gut sympathetic neurons. Retrograde polysynaptic neuronal tracing from the intestinal wall identifies brainstem sensory nuclei that are activated during microbial depletion, as well as efferent sympathetic premotor glutamatergic neurons that regulate gastrointestinal transit. These results reveal microbiota-dependent control of gut-extrinsic sympathetic activation through a gut-brain circuit.
Topics: Animals; Dysbiosis; Female; Ganglia, Sympathetic; Gastrointestinal Microbiome; Gastrointestinal Motility; Germ-Free Life; Intestines; Male; Mice; Mice, Inbred C57BL; Models, Animal; Neural Pathways; Neurons; Proto-Oncogene Proteins c-fos; Sympathetic Nervous System; Transcriptome
PubMed: 32641826
DOI: 10.1038/s41586-020-2474-7 -
Neuron Jan 2022Spontaneous pain refers to pain occurring without external stimuli. It is a primary complaint in chronic pain conditions and remains difficult to treat. Moreover, the...
Spontaneous pain refers to pain occurring without external stimuli. It is a primary complaint in chronic pain conditions and remains difficult to treat. Moreover, the mechanisms underlying spontaneous pain remain poorly understood. Here we employed in vivo imaging of dorsal root ganglion (DRG) neurons and discovered a distinct form of abnormal spontaneous activity following peripheral nerve injury: clusters of adjacent DRG neurons firing synchronously and sporadically. The level of cluster firing correlated directly with nerve injury-induced spontaneous pain behaviors. Furthermore, we demonstrated that cluster firing is triggered by activity of sympathetic nerves, which sprout into DRGs after injury, and identified norepinephrine as a key neurotransmitter mediating this unique firing. Chemogenetic and pharmacological manipulations of sympathetic activity and norepinephrine receptors suggest that they are necessary and sufficient for DRG cluster firing and spontaneous pain behavior. Therefore, blocking sympathetically mediated cluster firing may be a new paradigm for treating spontaneous pain.
Topics: Ganglia, Spinal; Humans; Pain; Sensory Receptor Cells; Spinal Nerves; Sympathetic Nervous System
PubMed: 34752775
DOI: 10.1016/j.neuron.2021.10.019 -
JAMA Psychiatry Feb 2020This is the first multisite, randomized clinical trial of stellate ganglion block (SGB) outcomes on posttraumatic stress disorder (PTSD) symptoms. (Randomized Controlled Trial)
Randomized Controlled Trial
IMPORTANCE
This is the first multisite, randomized clinical trial of stellate ganglion block (SGB) outcomes on posttraumatic stress disorder (PTSD) symptoms.
OBJECTIVE
To determine whether paired SGB treatments at 0 and 2 weeks would result in improvement in mean Clinician-Administered PTSD Scale for DSM-5 (CAPS-5) total symptom severity scores from baseline to 8 weeks.
DESIGN, SETTING, AND PARTICIPANTS
This multisite, blinded, sham-procedure, randomized clinical trial used a 2:1 SGB:sham ratio and was conducted from May 2016 through March 2018 in 3 US Army Interdisciplinary Pain Management Centers. Only physicians performing the procedures and the procedure nurses were aware of the intervention (but not the participants or assessors); their interactions with the participants were scripted and limited to the 2 interventions. Active-duty service members on stable psychotropic medication dosages who had a PTSD Checklist-Civilian Version (PCL-C) score of 32 or more at screening were included. Key exclusion criteria included a prior SGB treatment, selected psychiatric disorders or substance use disorders, moderate or severe traumatic brain injury, or suicidal ideation in the prior 2 months.
INTERVENTIONS
Paired right-sided SGB or sham procedures at weeks 0 and 2.
MAIN OUTCOMES AND MEASURES
Improvement of 10 or more points on mean CAPS-5 total symptom severity scores from baseline to 8 weeks, adjusted for site and baseline total symptom severity scores (planned a priori).
RESULTS
Of 190 screened individuals, 113 (59.5%; 100 male and 13 female participants; mean [SD] age, 37.3 [6.7] years) were eligible and randomized (74 to SGB and 39 to sham treatment), and 108 (95.6% of 113) completed the study. Baseline characteristics were similar in the SGB and sham treatment groups, with mean (SD) CAPS-5 scores of 37.6 (11.2) and 39.8 (14.4), respectively (on a scale of 0-80); 91 (80.0%) met CAPS-5 PTSD criteria. In an intent-to-treat analysis, adjusted mean total symptom severity score change was -12.6 points (95% CI, -15.5 to -9.7 points) for the group receiving SGB treatments, compared with -6.1 points (95% CI, -9.8 to -2.3 points) for those receiving sham treatment (P = .01).
CONCLUSIONS AND RELEVANCE
In this trial of active-duty service members with PTSD symptoms (at a clinical threshold and subthreshold), 2 SGB treatments 2 weeks apart were effective in reducing CAPS-5 total symptom severity scores over 8 weeks. The mild-moderate baseline level of PTSD symptom severity and short follow-up time limit the generalizability of these findings, but the study suggests that SGB merits further trials as a PTSD treatment adjunct.
TRIAL REGISTRATION
ClinicalTrials.gov identifier: NCT03077919.
Topics: Anesthetics, Local; Animals; Autonomic Nerve Block; Double-Blind Method; Female; Humans; Injections; Male; Psychiatric Status Rating Scales; Ropivacaine; Stellate Ganglion; Stress Disorders, Post-Traumatic
PubMed: 31693083
DOI: 10.1001/jamapsychiatry.2019.3474 -
Journal of Neuroimmunology Jan 2022After recovering from COVID-19, a significant proportion of symptomatic and asymptomatic individuals develop Long COVID. Fatigue, orthostatic intolerance, brain fog,...
After recovering from COVID-19, a significant proportion of symptomatic and asymptomatic individuals develop Long COVID. Fatigue, orthostatic intolerance, brain fog, anosmia, and ageusia/dysgeusia in Long COVID resemble "sickness behavior," the autonomic nervous system response to pro-inflammatory cytokines (Dantzer et al., 2008). Aberrant network adaptation to sympathetic/parasympathetic imbalance is expected to produce long-standing dysautonomia. Cervical sympathetic chain activity can be blocked with local anesthetic, allowing the regional autonomic nervous system to "reboot." In this case series, we successfully treated two Long COVID patients using stellate ganglion block, implicating dysautonomia in the pathophysiology of Long COVID and suggesting a novel treatment.
Topics: Adult; Autonomic Nerve Block; COVID-19; Female; Humans; SARS-CoV-2; Stellate Ganglion; Post-Acute COVID-19 Syndrome
PubMed: 34922127
DOI: 10.1016/j.jneuroim.2021.577784 -
Korean Journal of Critical Care Medicine Nov 2017Although methidathion is an organophosphate insecticide, it is different from the other organophosphates in terms of toxicity. Because of its relatively high fat...
Although methidathion is an organophosphate insecticide, it is different from the other organophosphates in terms of toxicity. Because of its relatively high fat solubility, the apparent volume of methidathion distribution throughout the body is very high, indicating that hemoperfusion is not effective in removing this organophosphate from the body. Redistribution of methidathion from fat to blood can also occur when plasma levels diminish. Additionally, acetylcholinesterase aging, which is the loss of an alkyl side chain that prevents reactivation by oximes, is very rapid so that the effective reactivation by oximes is thwarted. Thus, methidathion's effect on acetylcholinesterase inhibition is long lasting, particularly with a high dose. In addition to its parasympatholytic effect and ability to induce muscle paralysis, methidathion poisoning is associated with a profound and long-lasting circulatory collapse due to sympathetic ganglion blockade. This report presents the case of a 55-year-old man who accidentally ingested a high dose of methidathion. He later developed enteroinvasive aspergillosis infection-induced multiple bowel perforations on two separate occasions while on mechanical ventilator support, resulting in a fatal outcome. The renin-angiotensin axis activated by sympathetic ganglion blockade may have reduced the patient's splanchnic blood flow, contributing to translocation of endotoxin. Also, the effect of excessive acetylcholine on non-neuronal acetylcholine receptors may have contributed to the development of fatal enteroinvasive aspergillosis in this patient.
PubMed: 31723659
DOI: 10.4266/kjccm.2016.00073