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Animal models of predator defense distinguish qualitatively different behavioral modes that are activated at increasing levels of predation threat. A defense mode observed at intermediate threat levels is freezing: a cessation of locomotion that is characterized by a parasympathetically dominated autonomic nervous system response that causes heart rate deceleration, or fear bradycardia. Studies in rodents have shown that freezing depends on amygdalar projections to the periaqueductal grey (PAG). In humans, freezing-like behaviors are implicated in development and maintenance of psychopathology, but neural mechanisms underlying freezing or its characteristic autonomic response profile have not been identified. Here, we combined event-related blood oxygenation level-dependent functional MRI (BOLD-fMRI) with autonomic response measures in a picture viewing paradigm to probe activity and interconnectivity within the amygdala-PAG pathway and test for an association with parasympathetic as opposed to sympathetic activation. In response to negatively arousing pictures, we observed parasympathetic (bradycardia) and sympathetic (pupil dilation) autonomic responses, BOLD responses in the amygdala and PAG, and effective connectivity between these regions. Critically, BOLD responses in the PAG to negative pictures correlated on a trial-by-trial basis with bradycardia but not pupil dilation. This correlation with bradycardia remained significant when partialling out pupil dilation. Additionally, activity in regions associated with motor planning and inhibition mirrored the PAG response. Thus, our findings implicate the human PAG in a parasympathetically dominated defense mode that subserves a state of attentive immobility. Mechanistic insight into this qualitatively distinct defense mode may importantly advance translational models of anxiety disorders.
With the widespread use of alectinib in patients with anaplastic lymphoma kinase (ALK)-positive non-small-cell lung cancer (NSCLC), its cardiotoxicity has gradually emerged, including new-onset sinus bradycardia (SB). However, the incidence, timing, severity, and risk factors of alectinib-induced bradycardia remain unknown.
Remdesivir is an antiviral medication that is used in the treatment of severe COVID-19. Research has highlighted the potential cardiac side effects of remdesivir, including the occurrence of remdesivir-associated bradycardia (RAB), but these findings have not been consistent. In addition, very little is known about the clinical implications and outcomes of RAB. The aim of this rapid systematic review is to determine the event rate of developing bradycardia while receiving remdesivir treatment compared with not receiving remdesivir in patients diagnosed with COVID-19.
Electromuscular incapacitating devices (EMDs) are high-voltage, low-current stimulators causing involuntary muscle contractions and sensory response. Existing evidence about cardiac effects of EMD remains inconclusive. The aim of our study was to analyze electrocardiographic, echocardiographic, and microvolt T-wave alternans (MTWA) changes induced by EMD discharge.We examined 26 volunteers (22 men; median age 30 years) who underwent single standard 5-second duration exposure to TASER X26 under continuous echocardiographic and electrocardiographic monitoring. Microvolt T-wave alternans testing was performed at baseline (MTWA-1), as well as immediately and 60 minutes after EMD exposure (MTWA-2 and MTWA-3, respectively).Mean heart rate (HR) increased significantly from 88 ± 17 beats per minute before to 129 ± 17 beats per minute after exposure (P < 0.001). However, in 2 individuals, an abrupt decrease in HR was observed. In one of them, interval between two consecutive beats increased up to 1.7 seconds during the discharge. New onset of supraventricular premature beats was observed after discharge in 1 patient. Results of MTWA-1, MTWA-2, and MTWA-3 tests were positive in one of the subjects, each time in a different case.Standard EMD exposure can be associated with a nonuniform reaction of HR and followed by heart rhythm disturbances. New MTWA positivity can reflect either the effect of EMD exposure or a potential false positivity of MTWA assessments.
Lesions in the cerebellar vermis abolish acquisition of fear-conditioned bradycardia in animals and human patients. The δ2 glutamate receptor (GluD2) is predominantly expressed in cerebellar Purkinje cells. The mouse mutant ho15J carries a spontaneous mutation in GluD2 and these mice show a primary deficiency in parallel fiber-Purkinje cell synapses, multiple innervations of Purkinje cells by climbing fibers, and impairment of long-term depression. In the present study, we used ho15J mice to investigate the role of the cerebellum in fear-conditioned bradycardia. We recorded changes in heart rate of ho15J mice induced by repeated pairing of an acoustic (conditioned) stimulus (CS) with an aversive (unconditioned) stimulus (US). The mice acquired conditioned bradycardia on Day 1 of the CS-US phase, similarly to wild-type mice. However, the magnitude of the conditioned bradycardia was not stable in the mutant mice, but rather was exaggerated on Days 2-5 of the CS-US phase. We examined the effects of reversibly inactivating the cerebellum by injection of an antagonist against the α-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptor (AMPAR). The antagonist abolished expression of conditioned responses in both wild-type and ho15J mice. We conclude that the GluD2 mutation in the ho15J mice affects stable retention of the acquired conditioned bradycardia.
The inferior olive (IO) sends excitatory inputs to the cerebellar cortex and cerebellar nuclei through the climbing fibers. In eyeblink conditioning, a model of motor learning, the inactivation of or a lesion in the IO impairs the acquisition or expression of conditioned eyeblink responses. Additionally, climbing fibers originating from the IO are believed to transmit the unconditioned stimulus to the cerebellum in eyeblink conditioning. Studies using fear-conditioned bradycardia showed that the cerebellum is associated with adaptive control of heart rate. However, the role of inputs from the IO to the cerebellum in fear-conditioned bradycardia has not yet been investigated. To examine this possible role, we tested fear-conditioned bradycardia in mice by selective disruption of the IO using 3-acetylpyridine. In a rotarod test, mice with an IO lesion were unable to remain on the rod. The number of neurons of IO nuclei in these mice was decreased to ∼40% compared with control mice. Mice with an IO lesion did not show changes in the mean heart rate or in heart rate responses to a conditioned stimulus, or in their responses to a painful stimulus in a tail-flick test. However, they did show impairment of the acquisition/expression of conditioned bradycardia and attenuation of heart rate responses to a pain stimulus used as an unconditioned stimulus. These results indicate that the IO inputs to the cerebellum play a key role in the acquisition/expression of conditioned bradycardia.
Irisin is a newly identified hormone induced in muscle and adipose tissues by physical activity. This protein and its encoding gene have been identified in the brain; in addition, the precursor for irisin, FNDC5, can cross the blood-brain barrier. The fact that irisin is secreted during exercise together with the lower resting heart rate in athletes prompted us to investigate the effect of irisin on cardiac-projecting vagal neurons of nucleus ambiguus, a key regulatory site of heart rate. In vitro experiments in cultured nucleus ambiguus neurons indicate that irisin activates these neurons, inducing an increase in cytosolic Ca(2+) concentration and neuronal depolarization. In vivo microinjection of irisin into the nucleus ambiguus promotes bradycardia in conscious rats. Our study is the first to report the effects of irisin on the neurons controlling the cardiac vagal tone and to link a myokine to a cardioprotective role, by modulating central cardiovascular regulation.
Electroacupuncture (EA) stimulates somatic median afferents underlying P5-6 acupoints and modulates parasympathoexcitatory reflex responses through central processing in the brainstem. Although decreases in blood pressure and heart rate by the neural-mediated Bezold-Jarisch reflex responses are modulated by EA through opioid actions in the nucleus tractus solitarius and nucleus ambiguus, the role of the hypothalamus is unclear. The hypothalamic paraventricular nucleus (PVN) is activated by sympathetic afferents and regulates sympathetic outflow and sympathoexcitatory cardiovascular responses. In addition, the PVN is activated by vagal afferents, but little is known about its regulation of cardiopulmonary inhibitory hemodynamic responses. We hypothesized that the PVN participates in the Bezold-Jarisch reflex responses and EA inhibits these cardiopulmonary responses through the PVN opioid system. Rats were anesthetized and ventilated, and their heart rate and blood pressures were monitored. Application of phenylbiguanide every 10 min close to the right atrium induced consistent depressor and bradycardia reflex responses. Unilateral microinjection of the depolarization blockade agent kainic acid or glutamate receptor antagonist kynurenic acid in the PVN reduced these reflex responses. In at least 70% of the rats, 30 min of bilateral EA at P5-6 acupoints reduced the depressor and bradycardia responses for at least 60 min. Blockade of the CCK-1 receptors converted the non-responders into EA-responders. Unilateral PVN-microinjection with naloxone reversed the EA inhibition. Vagal-evoked activity of the PVN cardiovascular neurons was reduced by 30 min EA (P5-6) through opioid receptor activation. These data indicate that PVN processes inhibitory cardiopulmonary reflexes and participates in EA-modulation of the neural-mediated vasodepression and bradycardia.
Previous studies have shown that testosterone enhances baroreflex bradycardia. Therefore, conscious unrestrained rats were used to investigate the role of the androgen receptor in the testosterone-mediated modulation of baroreflex bradycardia. Androgen depletion (3 weeks), and androgen receptor blockade (20-24 h), were implemented to test the hypothesis that testosterone influences baroreflex bradycardia via its activity at the androgen receptor in male rats. Phenylephrine (1-16 microg kg(-1)) was used to assess baroreflex bradycardia.
We contrasted the forced diving bradycardia between two genetically similar (inbred) rat strains (Fischer and Buffalo), compared to that of outbred rats (Wistar). The animals were habituated to forced diving for 4 weeks. Each animal was then tested during one 40 s dive on each of 3 days. The heart rate (f(H)) was measured before, during, and after each dive. Fischer and Buffalo exhibited marked difference in dive bradycardia (Fischer: 120.9 ± 14.0 beats min(-1) vs. Buffalo: 92.8 ± 12.8 beats min(-1), P < 0.05). Outbred rats showed an intermediate response (103.0 ± 30.9 beats min(-1)) but their between-animal variability in mean dive f(H) and pre-diving resting f(H) were higher than the inbred strains (P < 0.05), which showed no difference (P > 0.05). The decreased variability in f(H) in inbred rats as compared with the outbred group indicates that reduced genetic variability minimizes variability of the diving bradycardia between individuals. Heritability within strains was assessed by the repeatability (R) index and was 0.93 ± 0.05 for the outbred, 0.84 ± 0.16 for Buffalo, and 0.80 ± 0.12 for Fischer rats for f(H) during diving. Our results suggest that a portion of the mammalian diving bradycardia may be a heritable trait.
Background and Objectives: Prematurity of birth occurs before the 37th week of gestation and affects up to 10% of births worldwide. It is correlated with critical outcomes; therefore, constant monitoring in neonatal intensive care units or home environments is required. The aim of this work was to develop solutions for remote neonatal intensive supervision systems, which should assist medical diagnosis of premature infants and raise alarm at cardiac abnormalities, such as bradycardia. Additionally, the COVID-19 pandemic has put a worldwide stress upon the medical staff and the management of healthcare units. Materials and Methods: A traditional medical diagnosing scheme was set up, implemented with the aid of powerful mathematical operators. The algorithm was tailored to the infants' personal ECG characteristics and was tested on real ECG data from the publicly available PhysioNet database "Preterm Infant Cardio-Respiratory Signals Database". Different processing problems were solved: noise filtering, baseline drift removal, event detection and compression of medical data using the à trous wavelet transform. Results: In all 10 available clinical cases, the bradycardia events annotated by the physicians were correctly detected using the RR intervals. Compressing the ECG signals for remote transmission, we obtained compression ratios (CR) varying from 1.72 to 7.42, with the median CR value around 3. Conclusions: We noticed that a significant amount of noise can be added to a signal while monitoring using standard clinical sensors. We tried to offer solutions for these technical problems. Recent studies have shown that persons infected with the COVID-19 disease are frequently reported to develop cardiovascular symptoms and cardiac arrhythmias. An automatic surveillance system (both for neonates and adults) has a practical medical application. The proposed algorithm is personalized, no fixed reference value being applied, and the algorithm follows the neonate's cardiac rhythm changes. The performance depends on the characteristics of the input ECG. The signal-to-noise ratio of the processed ECG was improved, with a value of up to 10 dB.
Bradycardia is initiated by the sinoatrial node (SAN), which is regulated by a coupled-clock system. Due to the clock coupling, reduction in the 'funny' current (If), which affects SAN automaticity, can be compensated, thus preventing severe bradycardia. We hypothesize that this fail-safe system is an inherent feature of SAN pacemaker cells and is driven by synergy between If and other ion channels. This work aimed to characterize the connection between membrane currents and their underlying mechanisms in SAN cells. SAN tissues were isolated from C57BL mice and Ca2+ signaling was measured in pacemaker cells within them. A computational model of SAN cells was used to understand the interactions between cell components. Beat interval (BI) was prolonged by 54 ± 18% (N = 16) and 30 ± 9% (N = 21) in response to If blockade, by ivabradine, or sodium current (INa) blockade, by tetrodotoxin, respectively. Combined drug application had a synergistic effect, manifested by a BI prolonged by 143 ± 25% (N = 18). A prolongation in the local Ca2+ release period, which reports on the level of crosstalk within the coupled-clock system, was measured and correlated with the prolongation in BI. The computational model predicted that INa increases in response to If blockade and that this connection is mediated by changes in T and L-type Ca2+ channels.
Older adults exhibit reduced physiological responses to beta-adrenergic stimulation and parasympathetic inhibition. This study aimed to investigate the effect of reducing the incidence of bradycardia in the atropine and ephedrine pretreatment group compared to the control group in older adults who received spinal anesthesia with intravenous dexmedetomidine. Overall, 102 older adults aged over 65 years were randomly divided into three groups, and saline (control group), atropine at 0.5 mg (atropine group), and ephedrine at 8 mg (ephedrine group) were administered intravenously to each group as pretreatment. Immediately after spinal anesthesia, dexmedetomidine loading and study drug injections were commenced. The primary outcome was the incidence of bradycardia (<50 beats per min) within 60 min following dexmedetomidine loading. The incidence of bradycardia requiring atropine treatment was significantly higher in the control group than in the atropine and ephedrine groups (27.3% vs. 6.1% and 8.8%, respectively; p = 0.035), and no difference was noted between the atropine and ephedrine groups. Therefore, if ephedrine or atropine is selected and used according to the patient’s condition and clinical situation, it may be helpful in preventing bradycardia during spinal anesthesia using dexmedetomidine in older patients.
Opioids are widely used medicinally as analgesics and abused for hedonic effects, actions that are each complicated by substantial risks such as cardiorespiratory depression. These drugs mimic peptides such as β-endorphin, which has a key role in endogenous analgesia. The β-endorphin in the central nervous system originates from pro-opiomelanocortin (POMC) neurons in the arcuate nucleus and nucleus of the solitary tract (NTS). Relatively little is known about the NTSPOMC neurons but their position within the sensory nucleus of the vagus led us to test the hypothesis that they play a role in modulation of cardiorespiratory and nociceptive control. The NTSPOMC neurons were targeted using viral vectors in a POMC-Cre mouse line to express either opto-genetic (channelrhodopsin-2) or chemo-genetic (Pharmacologically Selective Actuator Modules). Opto-genetic activation of the NTSPOMC neurons in the working heart brainstem preparation (n = 21) evoked a reliable, titratable and time-locked respiratory inhibition (120% increase in inter-breath interval) with a bradycardia (125±26 beats per minute) and augmented respiratory sinus arrhythmia (58% increase). Chemo-genetic activation of NTSPOMC neurons in vivo was anti-nociceptive in the tail flick assay (latency increased by 126±65%, p<0.001; n = 8). All effects of NTSPOMC activation were blocked by systemic naloxone (opioid antagonist) but not by SHU9119 (melanocortin receptor antagonist). The NTSPOMC neurons were found to project to key brainstem structures involved in cardiorespiratory control (nucleus ambiguus and ventral respiratory group) and endogenous analgesia (periaqueductal gray and midline raphe). Thus the NTSPOMC neurons may be capable of tuning behaviour by an opioidergic modulation of nociceptive, respiratory and cardiac control.
Aims. The present study tries to investigate the gene expression profile of bradycardia rabbits' hearts after SSYX (SSYX, a traditional Chinese medicine) treatment. Methods. Eighteen adult rabbits were randomly assigned in three groups: sham, model, and SSYX treatment groups. Heart rate was recorded in rabbits and total RNA was isolated from hearts. Gene expression profiling was conducted and quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR) was performed to confirm the gene expression results. Patch clamp using human induced pluripotent stem cell-derived cardiomyocytes was applied to record the calcium current in the presence of SSYX. Results. The mean RR interval reduced after six weeks due to the injury of the sinoatrial node in the model group. This effect was partially reversed by 4-week SSYX treatment. cDNA microarray demonstrated that genes related with pacemaker current, calcium ion homeostasis, and signaling were altered by SSYX treatment. Results from patch clamp demonstrated that SSYX reduced the calcium current which is consistent with gene expression results. Conclusion. The present study shows mRNA remodeling of bradycardia and demonstrates that SSYX is effective in treating bradycardia by reversing altered gene expression in bradycardia models. Reduced calcium current by SSYX also confirmed the gene expression results.
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