Reduction In Parasympathetic Tone Research Articles

Baroreflex and chemoreflex interaction in high-altitude exposure: possible role on exercise performance.

The hypoxic chemoreflex and the arterial baroreflex are implicated in the ventilatory response to exercise. It is well known that long-term exercise training increases parasympathetic and decreases sympathetic tone, both processes influenced by the arterial baroreflex and hypoxic chemoreflex function. Hypobaric hypoxia (i.e., high altitude [HA]) markedly reduces exercise capacity associated with autonomic reflexes. Indeed, a reduced exercise capacity has been found, paralleled by a baroreflex-related parasympathetic withdrawal and a pronounced chemoreflex potentiation. Additionally, it is well known that the baroreflex and chemoreflex interact, and during activation by hypoxia, the chemoreflex is predominant over the baroreflex. Thus, the baroreflex function impairment may likely facilitate the exercise deterioration through the reduction of parasympathetic tone following acute HA exposure, secondary to the chemoreflex activation. Therefore, the main goal of this review is to describe the main physiological mechanisms controlling baro- and chemoreflex function and their role in exercise capacity during HA exposure.

RR Variability in Acute Coronary Syndromes

Heart rate variability (HRV) is a simple measure that estimates cardiac autonomic modulation. Analysis in the time domain and frequency range of RR variability suggests that the negative prognosis of patients with acute myocardial infarction is related to the overall neuro-vegetative imbalance. The alteration of RR variability reflects the dysfunction of the autonomic nervous system and especially the reduction of parasympathetic tone. The results of this study confirm the association between the reduction of RR variability and the increased risk of adverse events and mortality after acute myocardial infarction. Moreover, it appears that RR variability is an independent predictor for atrial fibrillation. Keywords: RR variability, myocardial infarction, HRV, sudden cardiac death

Autonomic Nervous System Modifications During Wakefulness and Sleep in a Cohort of Patients with Acute Ischemic Stroke

Goal: The aims of our study were to investigate autonomic modifications in wakefulness and sleep in a cohort of patients with acute ischemic stroke and to evaluate whereas these modifications were dependent by sleep stage and stroke lateralization. Materials and Methods: We prospectively enrolled 42 patients (22 men and 20 women, mean age: 69.8 ± 11.3; range: 32-92 years) with acute ischemic stroke. All participants underwent a full-night polysomnography. As index of autonomic nervous system we used Heart Rate Variability (HRV), analyzed in wakefulness and during different sleep stages. First, we compared our cohort with a control group of 42 healthy subjects, matched for age and sex. Subsequently, we divided our cohort in 2 subgroups according stroke lateralization (21 right, 21 left) and compared with control population. Findings: We observed significant modifications of HRV parameters mainly for the right lesions. In particular, we observed a prevalent parasympathetic tone during the wake (low frequency/high frequency [LF/HF]: right: 2.99 ± 8.91; controls: 3.88 ± 3.42; P < .01) and during REM (LF/HF right: 0.03 ± 1.58; controls: 2.92 ± 3.97; P < .01) accompanied by a significant reduction of sympathetic tone during REM (LF right: 23.85 ± 44.42 n.u.; controls: 51.13 ± 32.25 n.u.; P < .01), and by a reduction of parasympathetic tone during N3 (HF right: 28.09 ± 37.67 n.u.; controls: 43.08 ± 68.39 n.u.; P < .01). Conclusions: Our study indicates that autonomic dysfunctions in acute ischemic stroke are prevalent in right-side lesions and strictly dependent by sleep-wake stage.

Reduction in Parasympathetic Tone During Sleep in Children With Habitual Snoring.

Introduction: Changes in the autonomic nervous system due to Obstructive Sleep Apnea (OSA) during the life span have been described. Some pediatric studies have shown cardiovascular effects in children who do not fit the criteria for OSA; namely children with mild sleep disordered breathing.Objective: We investigated heart rate variability (HRV) during sleep in children with chronic snoring and flow limitation events during sleep.Methods: Ten children and adolescents with chronic snoring and an apnea hypopnea index < 1, associated to high Respiratory Index, and 10 controls matched for age, gender, and Tanner stage were monitored following one night of habituation in the sleep laboratory. HRV was studied at each sleep stage. The time and frequency domains were calculated for each 5-min period.Results: All patients were chronic heavy snorers. They presented an apnea hypopnea index = 0.8, respiratory disturbance index = 10.2/h with lowest O2 saturation 96.1 ± 2.4%. The total power of HRV was decreased in all stages (p < 0.05). There was also a decrease in NN50 and pNN50 during all sleep stages compared to healthy controls (p = 0.0003 and p = 0.03, respectively).Conclusion: A reduction in parasympathetic tone was found in the patient group. This may represent an autonomic impairment during sleep in children with mild SDB. A reduction in HRV in children with habitual snoring could be associated with possible increases in cardiovascular risk in adulthood.Significance: The study indicates that children with habitual snoring have important parasympathetic tone changes during sleep.

Reduction in parasympathetic tone during sleep in children with mild sleep-disordered breathing

Reduction in parasympathetic tone during sleep in children with mild sleep-disordered breathing

Subacute pyridostigmine exposure increases heart rate recovery and cardiac parasympathetic tone in rats.

Heart rate recovery (HRR) describes the rapid deceleration of heart rate after strenuous exercise and is an indicator of parasympathetic tone. A reduction in parasympathetic tone occurs in patients with congestive heart failure, resulting in prolonged HRR. Acetylcholinesterase inhibitors, such as pyridostigmine, can enhance parasympathetic tone by increasing cholinergic input to the heart. The objective of this study was to develop a rodent model of HRR to test the hypothesis that subacute pyridostigmine administration decreases cholinesterase activity and accelerates HRR in rats. Ten days after implantation of radiotelemetry transmitters, male Sprague Dawley rats were randomized to control (CTL) or treated (PYR; 0.14mg/mL pyridostigmine in the drinking water, 29days) groups. Rats were exercised on a treadmill to record HRR, and blood samples were collected on days 0, 7, 14, and 28 of pyridostigmine administration. Total cholinesterase and acetylcholinesterase (AChE) activity in plasma was decreased by 32%-43% and 57%-80%, respectively, in PYR rats on days 7-28, while plasma butyrylcholinesterase activity did not significantly change. AChE activity in red blood cells was markedly reduced by 64%-66%. HRR recorded 1minute after exercise was higher in the PYR group on days 7, 14 and 28, and on day 7 when HRR was estimated at 3 and 5minutes. Autonomic tone was evaluated pharmacologically using sequential administration of muscarinic (atropine) and adrenergic (propranolol) blockers. Parasympathetic tone was increased in PYR rats as compared with the CTL group. These data support the study hypothesis that subacute pyridostigmine administration enhances HRR by increasing cardiac parasympathetic tone.

Knockdown of Bradykinin B1 Receptor Reduces Neuro‐inflammation and Prevents the Development of Salt‐Sensitive Hypertension

We previously reported that DOCA‐salt hypertension is associated with increased bradykinin B1 receptor (B1R) expression in the brain. In the present study, we tested the hypothesis that B1R knockdown prevents the development of hypertension. To test this hypothesis, wild‐type (WT) and B1R knockout (KO) mice were implanted with telemetry probes for conscious blood pressure (BP) monitoring. DOCA (1 mg/g, sc) was implanted following baseline BP recording and drinking water was replaced by 1% NaCl solution. Autonomic function was analyzed using a pharmacological method involving ip injection of propranolol (4 mg/kg) and atropine (1 mg/kg). Changes in heart rate (ΔHR) were used as index of sympathetic and parasympathetic tones. Baseline mean arterial pressure (MAP) was not different between WT and B1R KO mice (102±2 vs. 104±5 mmHg), nor were ΔHR following assessment of sympathetic (−73±6 vs. −75±15 beats/minute) or parasympathetic tone (+166±7 vs. +153±12 beats/minute). Three weeks after DOCA‐salt treatment, MAP was significantly increased in WT mice (138±3 mmHg, P&lt;0.01 vs. baseline). However, this increase was blunted in B1R KO mice (121±2 mmHg, P&lt;0.05 vs. WT+DOCA). In addition, DOCA‐salt mediated enhancement of cardiac sympathetic drive (increased bradycardia to propranolol, −145±21 beats/minutes, P&lt;0.01 vs. baseline) and reduction of parasympathetic tone (reduced tachycardia to atropine, +111±8 beats/minute, P&lt;0.01 vs. baseline) were normalized in B1R KO mice (−72±13 and +165±6 beats/minute, respectively, P&lt;0.05 vs. WT+DOCA). DOCA‐salt treatment resulted in sympathoexcitation in WT mice, as indicated by increased urinary norepinephrine levels (299±23 ng/ml, P&lt;0.05 vs. control), but this increase was blunted in B1R KO mice with DOCA (172±30 ng/ml, P&lt;0.05 vs. WT+DOCA). Moreover, pro‐inflammatory high‐mobility group box 1 (HMGB1) and cyclooxygenase 2 protein levels were significantly upregulated in the hypothalamus following DOCA treatment in WT mice (2.5 and 2 fold, respectively, P&lt;0.05 vs. control) but not in B1R KO mice. WT mice treated with DOCA‐salt showed increased inflammation as indicated by increased gene expression of TNF (3 fold, n=9, p&lt;0.001 vs. WT), IL‐1beta (8 fold, n=9, p&lt;0.001 vs. WT) and IL‐6 (5 fold, n=9, p&lt;0.01 vs. WT) in the hypothalamic paraventricular nucleus (PVN) which was attenuated in B1R KO mice. Taken together, these data suggest that B1R knockdown prevents the development of hypertension, possibly through decreased sympathetic activity, reducing HMGB1 expression, and diminishing its downstream neuroinflammatory cascade.Support or Funding Information15SDG25720021 (SS), NIH/NHLBI (HL093178) (EL), and P30GM106392

Changes in heart rate variability and QT variability during the first trimester of pregnancy

The risk of new-onset arrhythmia during pregnancy is high, presumably relating to changes in both haemodynamic and cardiac autonomic function. The ability to non-invasively assess an individual’s risk of developing arrhythmia during pregnancy would therefore be clinically significant. We aimed to quantify electrocardiographic temporal characteristics during the first trimester of pregnancy and to compare these with non-pregnant controls.Ninety-nine pregnant women and sixty-three non-pregnant women underwent non-invasive cardiovascular and haemodynamic assessment during a protocol consisting of various physiological states (postural manoeurvres, light exercise and metronomic breathing). Variables measured included stroke volume, cardiac output, heart rate, heart rate variability, QT and QT variability and QTVI (a measure of the variability of QT relative to that of RR).Heart rate (p < 0.0005, p < 0.0005, p < 0.0005) and cardiac output (p = 0.043, p < 0.0005, p < 0.0005) were greater in pregnant women in all physiological states (respectively for the supine position, light exercise and metronomic breathing state), whilst stroke volume was lower in pregnancy only during the supine position (p < 0.0005). QTe (Q wave onset to T wave end) and QTa (T wave apex) were significantly shortened (p < 0.05) and QTeVI and QTaVI were increased in pregnancy in all physiological states (p < 0.0005). QT variability (p < 0.002) was greater in pregnant women during the supine position, whilst heart rate variability was reduced in pregnancy in all states (p < 0.0005).Early pregnancy is associated with substantial changes in heart rate variability, reflecting a reduction in parasympathetic tone and an increase in sympathetic activity. QTVI shifted to a less favourable value, reflecting a greater than normal amount of QT variability. QTVI appears to be a useful method for quantifying changes in QT variability relative to RR (or heart rate) variability, being sensitive not only to physiological state but also to gestational age. We support the use of non-invasive markers of cardiac electrical variability to evaluate the risk of arrhythmic events in pregnancy, and we recommend the use of multiple physiological states during the assessment protocol.

Effect of anticonvulsant therapy for absence epilepsy on heart function.

Monitoring of the heart status during increasing stress-induced load allowed us to evaluate heart function after treatment of absence epilepsy with anticonvulsants of various types of action. Functional load against the background of treatment with lamotrigine or convulex had different effects on the dynamics of heart rate variability, hemodynamic parameters of the heart, and risk of life-threatening arrhythmias. The decrease in hemodynamic parameters and ischemic changes in the myocardium after convulex therapy occurred at a lower functional load associated with more pronounced reduction in parasympathetic tone and heart rate variability than after lamotrigine therapy. This suggests that the heart of animals treated with convulex has lower functional capacities and, therefore, stress-induced decompensation and prenosological status developed earlier.

Analysis of 24-hour heart rate variations in patients with epilepsy receiving antiepileptic drugs

ObjectiveThe goal of the study described here was to evaluate interictal heart rate variability (HRV) in young patients with epilepsy, a patient population in whom sudden unexpected death in epilepsy (SUDEP) is known to be more common. MethodsTwenty-four-hour ambulatory ECG Holter recordings of 37 patients (15–40years old) and 32 healthy controls were compared. ResultsAll of the time domain indices (SDNN, SDANN, RMSSD, and HRV triangular index) were significantly suppressed (P<0.001), and there was a marked reduction in parasympathetic tone (reduced HFnu,P<0.001) and an increase in sympathetic tone (increased LFnu and LF/HF ratio, P<0.001) in the patient group. Stepwise linear regression analysis revealed that polytherapy and epilepsy duration >10years were independent variables associated with a reduction in SDNN. ConclusionOur data suggest that the major determinants of suppressed SDNN are polytherapy and epilepsy duration >10years. Analysis of spectral measures of frequency domain indices suggests that an increased sympathetic tone in association with a decreased parasympathetic tone may constitute the mechanism underlying SUDEP in young people with epilepsy.

Heart rate variability in bipolar mania and schizophrenia

Background Autonomic nervous system (ANS) dysfunction and reduced heart rate variability (HRV) have been reported in a wide variety of psychiatric disorders, but have not been well characterized in bipolar mania. We recorded cardiac activity and assessed HRV in acutely hospitalized manic bipolar (BD) and schizophrenia (SCZ) patients compared to age- and gender-matched healthy comparison (HC) subjects. Method HRV was assessed using time domain, frequency domain, and nonlinear analyses in 23 manic BD, 14 SCZ, and 23 HC subjects during a 5 min rest period. Psychiatric symptoms were assessed by administration of the Brief Psychiatric Rating Scale (BPRS) and the Young Mania Rating Scale (YMRS). Results Manic BD patients demonstrated a significant reduction in HRV, parasympathetic activity, and cardiac entropy compared to HC subjects, while SCZ patients demonstrated a similar, but non-significant, trend towards lower HRV and entropy. Reduction in parasympathetic tone was significantly correlated with higher YMRS scores and the unusual thought content subscale on the BPRS. Decreased entropy was associated with increased aggression and diminished personal hygiene on the YMRS scale. Conclusion Cardiac function in manic BD individuals is characterized by decreased HRV, reduced vagal tone, and a decline in heart rate complexity as assessed by linear and nonlinear methods of analysis. Autonomic dysregulation is associated with more severe psychiatric symptoms, suggesting HRV dysfunction in this disorder may be dependent on the phase of the illness.

An Overview of the Effect of Weight Loss on Cardiovascular Autonomic Function

The prevalence of obesity is rising to epidemic proportions in many countries worldwide. Obesity seriously increases an individual's risk of developing many health problems including diabetes. Diabetes, like obesity, is also in epidemic proportions with 300 million adults predicted to have the disease by 2025. Investigating strategies for the prevention and treatment of obesity and diabetes is vitally important. Autonomic dysfunction is evident in both obesity and diabetes. In persons with diabetes, impaired cardiovascular autonomic activity is characterized by a reduction in parasympathetic tone with a relative increase in sympathetic activity and is specifically associated with a number of clinically significant manifestations including exercise intolerance, intraoperative cardiovascular lability, orthostatic hypotension, silent myocardial ischemia, and increased risk of mortality. In obesity, parasympathetic function is decreased while regional heterogeneity of increased sympathetic activity may occur. Autonomic dysfunction increases cardiovascular workload, hemodynamic stress, serious dysrhythmias, and significant cardiac pathology. Thus, cardiac autonomic imbalance may also be an important link between obesity and increased morbidity and mortality. Beyond the obese and diabetic state, multiple variables associated with these conditions such as insulin, glucose, leptin, adiponectin and free fatty acids have an affect on the autonomic nervous system. Autonomic disturbances, however, appear to be reversible with weight reduction. Since autonomic imbalance is a marker of adverse risk, improvement obtained from weight loss should be beneficial for the health of individuals with obesity and diabetes. This overview will examine the relationship of the autonomic nervous system in obesity and diabetes and explore the effect of weight loss on autonomic function.

Neuroanatomical correlates of voluntary inhibition of accommodation/vergence under monocular open‐loop viewing conditions

The purpose of this work is to identify human neural circuits involved in inhibition of accommodation/vergence by contrasting the cortical functions subservient to negative voluntary accommodation/vergence (NVA) with those evoked by active fixation in darkness (FIX). Five subjects with normal corrected acuity were studied using positron emission tomography and the HO bolus technique. The dominant right eye viewed a laser speckle pattern (633 nm) whose direction and velocity of motion were determined by the refractive state of the eye. The speckle pattern was presented at a distance of 1.8 m (0.55 D). The non-dominant eye was patched. Subjects performed two tasks counterbalanced for order effects: (i) attempted fixation on the remembered target in darkness with the dominant eye open and 'fixating'; and (ii) voluntary reduction of the laser speckle flow during each alternate 20-s epoch when a convex +2.0 D lens was placed in front of the right eye causing the speckle pattern to move downwards at 3 degrees /s. Comparison of the condition of NVA with the condition of FIX indicated widespread occipital activation. Decreases in absolute regional cerebral blood flow occurred in the superior parietal cortex (BA 5), frontal cortex (BA 8 and 10) and within the postcentral/precentral gyrus (BA 1/2/3/4) bilaterally where deactivation clusters eclipsed the presumed neck and shoulder areas. Negative accommodation/vergence appears to be driven by a reduction of parasympathetic tone, and has the effect of shutting down brain regions known to be involved in regulating visual search as well as a centrally controlled eye-head-neck-shoulder motor programme responsible for posturing gaze.

Autonomic involvement in multiple sclerosis: a pupillometric study.

To study pupillary autonomic function in multiple sclerosis (MS), we examined 36 subjects with low disability, preserved visual acuity and no recent history (2 years) of optic neuritis or actual visual complaints. Compared to controls, MS patients showed a greater dilatator reaction with darkness and, for the light reflex, a lower amplitude and contraction rate and a greater recovery of pupillary diameter 5 s after the stimulus. Within the MS group, no difference was found comparing patients with or without the following characteristics: nuclear magnetic resonance imaging evidence of midbrain lesions; increased visual evoked potential P100 latency; and a previous history of optic neuritis. No correlation was found between P100 latency, duration of disease and pupillometric parameters. Our results indicate that in MS patients there is autonomic dysfunction with a reduction of parasympathetic tone and a relative increase in sympathetic dilatator tone to the pupils. We suggest that pupillary abnormalities could be due to non-specific impairment of the central pathways subserving pupil functions.

Autonomic nervous control of heart rate in muskrats during exercise in air and under water.

Neural control of the cardiac responses to exercise in air (running) and under water (diving) was studied in the muskrat (Ondatra zibethicus) by means of acute pharmacological blockade with the muscarinic blocker atropine and the beta-adrenergic blocker nadolol. Saline injection was used as a control. Controls running on a treadmill showed a marked increase in heart rate with exercise. Atropine-treated animals had a higher resting heart rate than controls, but heart rate still increased with running. Nadolol-treated animals had a lower resting heart rate than controls and displayed a less pronounced increase in heart rate with running than controls. Animals treated with a combination of atropine and nadolol had a resting heart rate similar to that of controls but their heart rate was unaffected by running. Thus, exercise tachycardia in muskrats is due to activation of the sympathetic system and also to a reduction in parasympathetic tone. Heart rate decreased markedly during voluntary submergence in controls but rose as muskrats swam submerged against increasing water flows. Nevertheless, diving bradycardia was still present. Free-diving bradycardia and the relative increase in heart rate with underwater exercise were abolished by atropine and unaffected by nadolol. Hence, unlike the cardiac response to exercise in air, the cardiac response to underwater exercise is due only to a reduction in parasympathetic tone. Injection of the beta-adrenergic agonist isoproterenol markedly increased heart rate in air but had little effect during voluntary and forced dives, indicating a marked decrease in the sensitivity of cardiac cells to adrenergic stimulation during submergence. These results strongly suggest that accentuated antagonism between the two branches of the autonomic nervous system occurs during diving so that parasympathetic influences on the heart predominate and inhibit any chronotropic response to adrenergic stimulation.

Vagal tone in generalized anxiety disorder and the effects of aversive imagery and worrisome thinking

Vagal tone was assessed in 15 generalized anxiety disorder (GAD) and 15 nonanxious control participants during initial baseline, aversive imagery related to worry topics, worrisome thinking, and final baseline. The GAD group showed significantly lower vagal tone at initial baseline and little change over experimental tasks, suggesting the possibility of chronic reduction in parasympathetic tone. Nonanxious participants, on the other hand, displayed significant decreases in vagal tone from baseline to imagery and further reductions from imagery to worrisome thinking. Participants reported greater anxiety during worry than during aversive images but also greater ease of generation and maintenance of the worrisome thoughts. The results support prior theorizing that GAD is characterized by autonomic inflexibility, that this phenomenon is partly due to deficient parasympathetic tone, and that worrisome thinking in particular causes phasic reductions in vagal tone.