Showing papers on "Autonomic nervous system published in 2009"

Central and autonomic nervous system interaction is altered by short-term meditation

Abstract: Five days of integrative body–mind training (IBMT) improves attention and self-regulation in comparison with the same amount of relaxation training. This paper explores the underlying mechanisms of this finding. We measured the physiological and brain changes at rest before, during, and after 5 days of IBMT and relaxation training. During and after training, the IBMT group showed significantly better physiological reactions in heart rate, respiratory amplitude and rate, and skin conductance response (SCR) than the relaxation control. Differences in heart rate variability (HRV) and EEG power suggested greater involvement of the autonomic nervous system (ANS) in the IBMT group during and after training. Imaging data demonstrated stronger subgenual and adjacent ventral anterior cingulate cortex (ACC) activity in the IBMT group. Frontal midline ACC theta was correlated with high-frequency HRV, suggesting control by the ACC over parasympathetic activity. These results indicate that after 5 days of training, the IBMT group shows better regulation of the ANS by a ventral midfrontal brain system than does the relaxation group. This changed state probably reflects training in the coordination of body and mind given in the IBMT but not in the control group. These results could be useful in the design of further specific interventions.

The polyvagal theory: New insights into adaptive reactions of the autonomic nervous system

Abstract: QThe polyvagal theory describes an autonomic nervous system that is infl uenced by the central nervous system, sensitive to afferent infl uences, characterized by an adaptive reactivity dependent on the phylogeny of the neural circuits, and interactive with source nuclei in the brainstem regulating the striated muscles of the face and head. The theory is dependent on accumulated knowledge describing the phylogenetic transitions in the vertebrate autonomic nervous system. Its specifi c focus is on the phylogenetic shift between reptiles and mammals that resulted in specifi c changes to the vagal pathways regulating the heart. As the source nuclei of the primary vagal efferent pathways regulating the heart shifted from the dorsal motor nucleus of the vagus in reptiles to the nucleus ambiguus in mammals, a face‐heart connection evolved with emergent properties of a social engagement system that would enable social interactions to regulate visceral state.

Influence of Mental Stress on Heart Rate and Heart Rate Variability

Abstract: Stress is a huge problem in today’s society. Being able to measure stress, therefore, may help to address this problem. Although stress has a psychological origin, it affects several physiological processes in the human body: increased muscle tension in the neck, change in concentration of several hormones and a change in heart rate (HR) and heart rate variability (HRV). The brain innervates the heart by means of stimuli via the Autonomic Nervous System (ANS), which is divided into sympathetic and parasympathetic branches. The sympathetic activity leads to an increase in HR (e.g. during sports exercise), while parasympathetic activity induces a lower HR (e.g. during sleep). The two circuits are constantly interacting and this interaction is reflected in HRV. HRV, therefore, provides a measure to express the activity of the ANS, and may consequently provide a measure for stress. We therefore explored measures of HR and HRV with an imposed stressful situation. We recorded changes in HR and HRV in a group of 28 subjects at rest, and with a mental stressor. The results suggest that HR and HRV change with a mental task. HR and HRV recordings may have the potential, therefore, to measure stress levels and guide preventive measures to reduce stress related illnesses.

Growth retardation and altered autonomic control in mice lacking brain serotonin.

Abstract: Serotonin synthesis in mammals is initiated by 2 distinct tryptophan hydroxylases (TPH), TPH1 and TPH2. By genetically ablating TPH2, we created mice (Tph2−/−) that lack serotonin in the central nervous system. Surprisingly, these mice can be born and survive until adulthood. However, depletion of serotonin signaling in the brain leads to growth retardation and 50% lethality in the first 4 weeks of postnatal life. Telemetric monitoring revealed more extended daytime sleep, suppressed respiration, altered body temperature control, and decreased blood pressure (BP) and heart rate (HR) during nighttime in Tph2−/− mice. Moreover, Tph2−/− females, despite being fertile and producing milk, exhibit impaired maternal care leading to poor survival of their pups. These data confirm that the majority of central serotonin is generated by TPH2. TPH2-derived serotonin is involved in the regulation of behavior and autonomic pathways but is not essential for adult life.

Antecedent hypoglycemia impairs autonomic cardiovascular function - implications for rigorous glycemic control

Abstract: OBJECTIVE— Glycemic control decreases the incidence and progression of diabetic complications but increases the incidence of hypoglycemia. Hypoglycemia can impair hormonal and autonomic responses to subsequent hypoglycemia. Intensive glycemic control may increase mortality in individuals with type 2 diabetes at high risk for cardiovascular complications. We tested the hypothesis that prior exposure to hypoglycemia leads to impaired cardiovascular autonomic function. RESEARCH DESIGN AND METHODS— Twenty healthy subjects (age 28 ± 2 years; 10 men) participated in two 3-day inpatient visits, separated by 1–3 months. Autonomic testing was performed on days 1 and 3 to measure sympathetic, parasympathetic, and baroreflex function. A 2-h hyperinsulinemic [hypoglycemic (2.8 mmol/l) or euglycemic (5.0 mmol/l)] clamp was performed in the morning and in the afternoon of day 2. RESULTS— Comparison of the day 3 autonomic measurements demonstrated that antecedent hypoglycemia leads to 1 ) reduced baroreflex sensitivity (16.7 ± 1.8 vs. 13.8 ± 1.4 ms/mmHg, P = 0.03); 2 ) decreased muscle sympathetic nerve activity response to transient nitroprusside-induced hypotension (53.3 ± 3.7 vs. 40.1 ± 2.7 bursts/min, P 3 ) reduced ( P CONCLUSIONS— Baroreflex sensitivity and the sympathetic response to hypotensive stress are attenuated after antecedent hypoglycemia. Because impaired autonomic function, including decreased cardiac vagal baroreflex sensitivity, may contribute directly to mortality in diabetes and cardiovascular disease, our findings raise new concerns regarding the consequences of hypoglycemia.

The role of cardiac autonomic function in hypertension and cardiovascular disease

Abstract: Autonomic nervous system abnormality, clinically manifested as a hyperkinetic circulation characterized by elevations in heart rate, blood pressure, plasma norepinephrine levels, and cardiac output, has been repeatedly demonstrated in hypertension. Increased release of norepinephrine from the brain has also been described in hypertension, and increased sympathetic activity has been demonstrated using spectral analysis of heart rate variability, particularly in the early stage of hypertension and in white-coat hypertension. Studies performed with microneurographic assessment also have found a marked increase in muscle sympathetic nervous activity in subjects with both borderline and established hypertension. A transition from the early hyperkinetic state to a high-resistance, established hypertension has been documented in longitudinal studies. The high blood pressure induces vascular hypertrophy, which in turn leads to increased vascular resistance. Cardiac output returns from elevated to normal values as β-adrenergic receptors are downregulated and stroke volume decreases. In parallel with the hemodynamic transition, the sympathetic tone is reset in the course of hypertension. Autonomic nervous system abnormality is also associated with such pressure-unrelated cardiovascular risk factors as tachycardia, high hematocrit, insulin resistance, and obesity. Mechanisms of this association are discussed.

Nesfatin-1 exerts cardiovascular actions in brain: possible interaction with the central melanocortin system.

Abstract: Nesfatin-1 is a recently discovered hypothalamic peptide that was shown to suppress food intake through a melanocortin-3/4 receptor-dependent mechanism. Since nesfatin-1 mRNA is detected in the paraventricular nucleus of the hypothalamus, and because many peptides that alter food intake also influence cardiovascular function, we tested the ability of centrally administered nesfatin-1 to affect mean arterial pressure (MAP) in conscious, freely moving rats. Significant increases in MAP were observed following intracerebroventricular administration of nesfatin-1. Pretreatment with either the melanocortin-3/4 receptor antagonist, SHU9119 (intracerebroventricular), or the α-adrenergic antagonist, phentolamine (intra-arterial), abrogated the rise in MAP induced by nesfatin-1, indicating that nesfatin-1 may interact with the central melanocortin system to increase sympathetic nerve activity and lead to an increase in MAP. Thus we have identified a novel action of nesfatin-1, in addition to its anorexigenic effects, to stimulate autonomic nervous system activity.

Peptide neurons in peripheral tissues including the urinary tract: immunohistochemical studies.

Abstract: Using the indirect immunofluorescence technique of Coons and collaborators, neurons containing substance P-, enkephalin-, vasoactive intestinal polypeptide (VIP) – and somatostatin-like immuno-reactivity have been identified in the peripheral nervous system. They have a widespread distribution, particulary in the gastrointestinal and urinary tracts. Whereas part of these peptide containing fibres may belong to sensory neurons, the majority seem to have their origin in peripheral autonomic ganglia, indicating a complex built up of the autonomic nervous system. There is evidence that some noradrenergic neurons contain somatostatin, which may suggest that one neuron can synthesize and store two transmitters. The significance of such neurons, as well as of peripheral peptide neurons in general, remains to be elucidated.

Analysis of heart rate variability

Abstract: Heart rate variability (HRV) is a measure of the beat-to-beat variations in heart rate. It is usually calculated by analyzing a time series of beat-to-beat intervals from the ECG. Various measures of heart rate variability have been proposed, which can be subdivided into time domain, frequency domain and non-linear measures. HRV is regarded as an indicator of the activity of autonomic regulation of circulatory function. HRV has considerable potential to assess the role of autonomic nervous system fluctuations in normal healthy individuals, in patients with various cardiovascular and noncardiovascular disorders and, in patients undergoing general anesthesia. HRV studies should enhance our understanding of physiological phenomena, perioperative cardiovascular changes, the actions of medications, and disease mechanisms.

Dose-response relationship of autonomic nervous system responses to individualized training impulse in marathon runners

Abstract: In athletes, exercise training induces autonomic nervous system (ANS) adaptations that could be used to monitor training status. However, the relationship between training and ANS in athletes has b...

Moderate pressure massage elicits a parasympathetic nervous system response

Abstract: Twenty healthy adults were randomly assigned to a moderate pressure or a light pressure massage therapy group, and EKGs were recorded during a 3-min baseline, during the 15-min massage period and during a 3-min postmassage period. EKG data were then used to derive the high frequency (HF), low frequency (LF) components of heart rate variability and the low to high frequency ratio (LF/HF) as noninvasive markers of autonomic nervous system activity. The participants who received the moderate pressure massage exhibited a parasympathetic nervous system response characterized by an increase in HF, suggesting increased vagal efferent activity and a decrease in the LF/HF ratio, suggesting a shift from sympathetic to parasympathetic activity that peaked during the first half of the massage period. On the other hand, those who received the light pressure massage exhibited a sympathetic nervous system response characterized by decreased HF and increased LF/HF.

Body mass index is related to autonomic nervous system activity as measured by heart rate variability

Abstract: Autonomic nervous system activity is involved in body weight regulation. We assessed whether the body mass index (BMI) is related to the autonomic nervous system activity as assessed by heart rate variability (HRV). Twenty-five adult normotensive, euglycemic healthy males (M) and females (F) were studied (M/F=13/12). BMI was assessed in each individual. HRV was assessed and the domains of low frequencies (LF, index of the sympathetic modulation) and high frequencies (HF, index of the parasympathetic modulation) were measured. Data were statistically analyzed and are presented as mean±s.d. Mean BMI did not correlate with either HF or LF. It inversely related to HF (r=−0.50, P<0.01), whereas its relationship with LF was marginally significant (r=−0.39, P=0.05). The HF in individuals with BMI <20 kg/m2 was significantly higher from those measured in the remaining subjects (P<0.05). The results support the role of parasympathetic activity in influencing BMI through likely modulation of body weight.

Impaired regulation of cardiac function in sepsis, SIRS, and MODS.

Abstract: In sepsis, systemic inflammatory response syndrome (SIRS), and multiorgan dysfunction syndrome (MODS), a severe prognostically relevant cardiac autonomic dysfunction exists, as manifested by a strong attenuation of sympatheti- cally and vagally mediated heart rate variability (HRV) The mechanisms underlying this attenuation are not limited to the nervous system They also include alterations of the cardiac pacemaker cells on a cellular level As shown in human atrial cardiomyocytes, endotoxin interacts with cardiac hyperpolarization-activated cyclic nucleotide-gated (HCN) ion channels, which mediate the pacemaker current If and play an important role in transmitting sympathetic and vagal signals on heart rate and HRV Moreover, endotoxin sensitizes cardiac HCN channels to sympathetic signals These findings identify endo- toxin as a pertinent modulator of the autonomic nervous regulation of heart function In MODS, the vagal pathway of the autonomic nervous system is particularly compromised, leading to an attenuation of the cholinergic antiinflammatory re- flex An amelioration of the blunted vagal activity appears to be a promising novel therapeutic target to achieve a suppres- sion of the inflammatory state and thereby an improvement of prognosis in MODS patients Preliminary data revealed therapeutic benefits (increased survival rates and improvements of the depressed vagal activity) of the administration of statins, b-blockers, and angiotensin-converting enzyme inhibitors in patients with MODS

Heart rate variability, overnight urinary norepinephrine and C‐reactive protein: evidence for the cholinergic anti‐inflammatory pathway in healthy human adults

Abstract: . Objectives. C-reactive protein (CRP) has been identified as an independent predictor of cardiovascular mortality and morbidity in population-based studies. Recent advances have suggested a prominent role for the autonomic nervous system (ANS) in the regulation of inflammation. However, no in vivo human studies have examined indices of sympathetic and parasympathetic nervous system activity simultaneously in relationship to inflammatory markers in apparently healthy adults. Therefore, the objective of this study was to assess the immunomodulatory effects of the ANS. Methods and results. The study population comprised 611 apparently healthy employees of an airplane manufacturing plant in southern Germany. Urinary NE was positively associated with white blood cell count (WBC) in the total sample. We found an inverse association between indices of vagally mediated heart rate variability and plasma levels of (CRP), which was significantly larger in females than in males after controlling for relevant covariates including NE. Similar results were found using the percentage of interbeat interval differences >50 ms and WBC. Conclusions. We report here for the first time, in a large sample of healthy human adults, evidence supporting the hypothesis of a clinically relevant cholinergic anti-inflammatory pathway after controlling for sympathetic nervous system activity. This suggests an important role for the vagal control of systemic inflammatory activity in cardiovascular disease.

Effects of nocturnal light on (clock) gene expression in peripheral organs: a role for the autonomic innervation of the liver.

Abstract: Background The biological clock, located in the hypothalamic suprachiasmatic nucleus (SCN), controls the daily rhythms in physiology and behavior. Early studies demonstrated that light exposure not only affects the phase of the SCN but also the functional activity of peripheral organs. More recently it was shown that the same light stimulus induces immediate changes in clock gene expression in the pineal and adrenal, suggesting a role of peripheral clocks in the organ-specific output. In the present study, we further investigated the immediate effect of nocturnal light exposure on clock genes and metabolism-related genes in different organs of the rat. In addition, we investigated the role of the autonomic nervous system as a possible output pathway of the SCN to modify the activity of the liver after light exposure. Methodology and Principal Findings First, we demonstrated that light, applied at different circadian times, affects clock gene expression in a different manner, depending on the time of day and the organ. However, the changes in clock gene expression did not correlate in a consistent manner with those of the output genes (i.e., genes involved in the functional output of an organ). Then, by selectively removing the autonomic innervation to the liver, we demonstrated that light affects liver gene expression not only via the hormonal pathway but also via the autonomic input. Conclusion Nocturnal light immediately affects peripheral clock gene expression but without a clear correlation with organ-specific output genes, raising the question whether the peripheral clock plays a “decisive” role in the immediate (functional) response of an organ to nocturnal light exposure. Interestingly, the autonomic innervation of the liver is essential to transmit the light information from the SCN, indicating that the autonomic nervous system is an important gateway for the SCN to cause an immediate resetting of peripheral physiology after phase-shift inducing light exposures.

Autonomic Neurotransmission: 60 Years Since Sir Henry Dale

Abstract: In the early twentieth century, Sir Henry Dale and others described brilliant studies of autonomic neurotransmission utilizing acetylcholine and noradrenaline. However, within the past 60 years, new discoveries have changed our understanding of the organization of the autonomic nervous system, including the structure and function of the nonsynaptic autonomic neuroeffector junction, the multiplicity of neurotransmitters, cotransmission, neuromodulation, dual control of vascular tone by perivascular nerves and endothelial cells, the molecular biology of receptors, and trophic signaling. Further, it is now recognized that an outstanding feature of autonomic neurotransmission is the inherent plasticity afforded by its structural and neurochemical organization and the interaction between expression of neural mediators and environmental factors. In this way, autonomic neurotransmission is matched to ongoing changes in demands and can sometimes be compensatory in pathophysiological situations.

Autonomic function and prognosis

Abstract: Autonomic nervous system function is assessed in the clinic by measuring resting heart rate, heart rate variability, or heart rate recovery following exercise. Each of these measures is a strong predictor of cardiovascular risk and all-cause mortality in primary and secondary prevention settings. These measures have been used to identify correlates of autonomic nervous system dysfunction at both the patient level (eg, obesity, diabetes, heart failure) and the environmental level (eg, smoking, social stress, air pollution). Future research must determine how to exploit the associations between autonomic system dysfunction and poor prognosis to improve patient outcomes.

Control of heart rate by cAMP sensitivity of HCN channels

Abstract: “Pacemaker” f-channels mediating the hyperpolarization-activated nonselective cation current If are directly regulated by cAMP. Accordingly, the activity of f-channels increases when cellular cAMP levels are elevated (e.g., during sympathetic stimulation) and decreases when they are reduced (e.g., during vagal stimulation). Although these biophysical properties seem to make f-channels ideal molecular targets for heart rate regulation by the autonomic nervous system, the exact contribution of the major If-mediating cardiac isoforms HCN2 and HCN4 to sinoatrial node (SAN) function remains highly controversial. To directly investigate the role of cAMP-dependent regulation of hyperpolarization activated cyclic nucleotide activated (HCN) channels in SAN activity, we generated mice with heart-specific and inducible expression of a human HCN4 mutation (573X) that abolishes the cAMP-dependent regulation of HCN channels. We found that hHCN4–573X expression causes elimination of the cAMP sensitivity of If and decreases the maximum firing rates of SAN pacemaker cells. In conscious mice, hHCN4–573X expression leads to a marked reduction in heart rate at rest and during exercise. Despite the complete loss of cAMP sensitivity of If, the relative extent of SAN cell frequency and heart rate regulation are preserved. Our data demonstrate that cAMP-mediated regulation of If determines basal and maximal heart rates but does not play an indispensable role in heart rate adaptation during physical activity. Our data also reveal the pathophysiologic mechanism of hHCN4–573X–linked SAN dysfunction in humans.

Influences of autonomic nervous system on atrial arrhythmogenic substrates and the incidence of atrial fibrillation in diabetic heart.

Abstract: Diabetes mellitus (DM) is clinically associated with an increased incidence of atrial fibrillation (AF), but the underlying mechanism remains unclear. We hypothesized that neural remodeling enhances AF vulnerability in diabetic hearts. Eight weeks after creating streptozotocin-induced diabetic rats (DM rats) or control rats, the hearts were perfused according to the Langendorff method. Inducibility of AF was evaluated by 5 times burst pacing from the right atrium and the atrial effective refractory period (AERP) was measured. The protocol was repeated during sympathetic nerve stimulation (SNS) or parasympathetic nerve stimulation (PNS). In tissue samples taken from the right atrium, the density of nerves positive for tyrosine hydroxylase (TH) and acetylcholinesterase (AChE) were determined. SNS significantly increased the incidence of AF in DM rats (14 +/- 6 to 30 +/- 8%, P < 0.01), but not in control rats (11 +/- 4 to 14 +/- 6%, NS). Although AERP was significantly decreased by SNS in both rats (each P < 0.01), increased heterogeneity of AERP by SNS was seen only in DM rats. PNS significantly decreased AERP and increased the incidence of AF (9 +/- 5 to 30 +/- 5% in control rats, 12 +/- 6 to 27 +/- 6% in DM rats, each P < 0.01) in both rats. The density of TH-positive nerves was heterogeneous in DM rats compared with control rats, whereas the heterogeneity of AChE-positive nerves was not different in the rats. The prevalence of AF was enhanced by adrenergic activation in diabetic hearts, in which heterogeneous sympathetic innervation was evident. These results suggest that neural remodeling may play a crucial role for increased AF vulnerability in DM.

Autonomic circulatory control during pregnancy in humans.

Abstract: Pregnancy is associated with dramatic alterations in maternal hemodynamics, which begin as early as 4 to 5 weeks of gestation. It has been proposed that these changes occur through autonomic control mechanisms, but the actual role of the autonomic nervous system in pregnancy is poorly understood. Here, we review what is known about the hemodynamic adaptation, changes in vascular endothelial function, sympathetic neural control and vascular responsiveness in pregnancy, and baroreflex function during pregnancy in humans. However, whether and how the sympathetic nervous system plays a role in hemodynamic homeostasis during EARLY human pregnancy remains completely unknown. Understanding the pathophysiology underlying autonomic control of maternal hemodynamics may be particularly important for prevention of cardiovascular complications during pregnancy and may improve risk stratification and prevention of cardiovascular disease for women well beyond the postpartum period.

Autonomic ganglia, acetylcholine receptor antibodies, and autoimmune ganglionopathy.

Abstract: Nicotinic acetylcholine receptors (AChR) are ligand-gated cation channels that are present throughout the nervous system. The ganglionic (α3-type) neuronal AChR mediates fast synaptic transmission in sympathetic, parasympathetic and enteric autonomic ganglia. Autonomic ganglia are an important site of neural integration and regulation of autonomic reflexes. Impaired cholinergic ganglionic synaptic transmission is one important cause of autonomic failure. Ganglionic AChR antibodies are found in many patients with autoimmune autonomic ganglionopathy (AAG). These antibodies recognize the α3 subunit of the ganglionic AChR, and thus do not bind non-specifically to other nicotinic AChR. Patients with high levels of ganglionic AChR antibodies typically present with rapid onset of severe autonomic failure, with orthostatic hypotension, gastrointestinal dysmotility, anhidrosis, bladder dysfunction and sicca symptoms. Impaired pupillary light reflex is often seen. Like myasthenia gravis, AAG is an antibody-mediated neurological disorder. Antibodies from patients with AAG inhibit ganglionic AChR currents and impair transmission in autonomic ganglia. An animal model of AAG in the rabbit recapitulates the important clinical features of the human disease and provides additional evidence that AAG is an antibody-mediated disorder caused by impairment of synaptic transmission in autonomic ganglia.

Cardiac dysfunctions following spinal cord injury

Abstract: The aim of this article is to analyze cardiac dysfunctions occurring after spinal cord injury (SCI). Cardiac dysfunctions are common complications following SCI. Cardiovascular disturbances are the leading causes of morbidity and mortality in both acute and chronic stages of SCI. We reviewed epidemiology of cardiac disturbances after SCI, and neuroanatomy and pathophysiology of autonomic nervous system, sympathetic and parasympathetic. SCI causes disruption of descendent pathways from central control centers to spinal sympathetic neurons, originating into intermediolateral nuclei of T1-L2 spinal cord segments. Loss of supraspinal control over sympathetic nervous system results in reduced overall sympathetic activity below the level of injury and unopposed parasympathetic outflow through intact vagal nerve. SCI associates significant cardiac dysfunction. Impairment of autonomic nervous control system, mostly in patients with cervical or high thoracic SCI, causes cardiac dysrrhythmias, especially bradycardia and, rarely, cardiac arrest, or tachyarrhytmias and hypotension. Specific complication dependent on the period of time after trauma like spinal shock and autonomic dysreflexia are also reviewed. Spinal shock occurs during the acute phase following SCI and is a transitory suspension of function and reflexes below the level of the injury. Neurogenic shock, part of spinal shock, consists of severe bradycardia and hypotension. Autonomic dysreflexia appears during the chronic phase, after spinal shock resolution, and it is a life-threatening syndrome of massive imbalanced reflex sympathetic discharge occurring in patients with SCI above the splanchnic sympathetic outflow (T5-T6). Besides all this, additional cardiac complications, such as cardiac deconditioning and coronary heart disease may also occur. Proper prophylaxis, including nonpharmacologic and pharmacological strategies and cardiac rehabilitation diminish occurrence of the cardiac dysfunction following SCI. Each type of cardiac disturbance requires specific treatment.