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PubMed1999

Junctional tachycardia during radiofrequency ablation of the slow pathway in patients with AV nodal reentrant tachycardia: effects of autonomic blockade.

INTRODUCTION: The autonomic nervous system richly innervates the peri-AV nodal region and may be activated during radiofrequency (RF) ablation for AV nodal reentrant tachycardia, resulting in the generation of junctional tachycardia. The purpose of this prospective study was to determine the role of the autonomic nervous system in the genesis of junctional tachycardia. METHODS AND RESULTS: We compared the characteristics of junctional tachycardia in patients with (n = 10) and without (n = 10) autonomic blockade undergoing RF ablation for AV nodal reentrant tachycardia. Intravenous administration of atropine (0.04 mg/kg) and propranolol (0.2 mg/kg) were used to block the autonomic nervous system. There were no differences in clinical variables and baseline electrophysiologic characteristics between the two groups except for slightly longer effective refractory periods of the fast pathway and of the atrium in the autonomic blockade group. The autonomic blockade shortened the baseline sinus cycle length and effective refractory period of the ventricle only but not other electrophysiologic characteristics of the AV node. The junctional tachycardia was observed during ablation in each patient, but its occurrence and cycle length, as well as numbers of consecutive junctional beats, were not altered by the autonomic blockade. CONCLUSION: Our results indicate that the muscarinic and beta-adrenergic components of the autonomic nervous system play no role in the genesis of junctional tachycardia.

Atrioventricular Node↗
PubMedDate not supplied

Clinical studies of autonomic function and dysfunction.

A discussion of progressive autonomic failure in man. This is one of the few neurological diseases disrupting cardiovascular function. Both central and peripheral pathways are involved. Means of diagnosing defects in autonomic reactions are described. Abnormalities in responses due to multiple system atrophy (MSA) are discussed most extensively.

Afferent Pathways↗
PubMed1999

Role of nitric oxide in the regulation of cardiovascular autonomic control.

Alteration in function of the cardiac autonomic nervous system has proved to be a powerful predictor of cardiac death or serious arrhythmia in patients with cardiac disease, yet little is known about the mechanisms by which this system is regulated. Recent evidence suggests that the gaseous molecule nitric oxide (NO) may act as an important mediator in this pathway. Histochemical staining techniques have identified neuronal populations that contain NO synthase within medullary cardio-regulatory sites and their peripheral autonomic pathways. Drugs that modulate the NO pathway (administered both systemically and into the central nervous system) cause changes in pre- and post-ganglionic sympathetic nerve activity that imply that NO serves to inhibit central sympathetic outflow. There is also evidence that NO may attenuate cardiovascular end-organ responses to sympathetic stimulation. Studies suggest that NO modulates cardiac vagal control, increasing the activity of central vagal motoneurons and, more contentiously, contributing to the bradycardic effects of vagal stimulation. NO also modulates so-called 'indirect' vagal inhibition of sympathetic cardiac responses. Additionally, central attenuation of baroreflex-mediated vagal control has been described. There is relatively little information available on the importance of NO in the regulation of human cardiovascular autonomic control. Further well-controlled studies are required.

Autonomic Nervous System↗
PubMed1993

Metabotropic glutamate receptors depress afferent excitatory transmission in the rat nucleus tractus solitarii.

1. We have previously demonstrated that the metabotropic glutamate receptor (mGluR) agonist (1S,3R)-1-aminocyclopentane-1,3-dicarboxylate [(1S;3R)-ACPD] presynaptically inhibits evoked glutamatergic excitatory postsynaptic currents (EPSCs) in patch-clamped rat nucleus tractus solitarius (NTS) neurons recorded in thin slices. The present study investigated the ability of endogenously released glutamate to modulate EPSCs in the NTS. 2. A low-frequency tetanus of the tractus solitarius (TS) resulted in either posttetanic potentiation (PTP) (8 of 21 cells) or depression (13 of 21 cells) of monosynaptic EPSCs recorded in the presence of D(-)2-amino-5-phosphonopentanoic acid (AP5) and bicuculline. 3. The amplitude of the EPSC was not significantly affected by the bath application of the mGluR antagonist (+) alpha-methyl-4-carboxyphenylglycine (MCPG). 4. In the presence of MCPG, a low-frequency tetanus resulted in PTP of the EPSC in all neurons. PTP was significantly enhanced in those cells previously exhibiting PTP. 5. The results suggest that presynaptic mGluRs on TS projections to the NTS may be activated by endogenously released glutamate at physiologically relevant stimulus frequencies and therefore play a role in the modulation of autonomic afferent transmission.

Afferent Pathways↗
PubMedDate not supplied

To stand on one's own legs.

A fundamental human expectation is to stand upright. This exposes the cardiovascular system to gravitational forces, with a fall in pressure above heart level exposing organs such as the brain to impaired perfusion if adequate adaptive mechanisms are not activated. The autonomic nervous system plays an important role in the initial response to standing upright, and can be affected by several disorders, some rare, some common. Autonomic failure can result in orthostatic hypotension with hypoperfusion of vital organs, causing a variety of symptoms including syncope. Thus, it is important to recognise orthostatic hypotension, determine its aetiology, evaluate and treat it. Intermittent autonomic dysfunction (such as neurally mediated syncope without chronic neurogenic failure) also results in falls and syncope; various forms include the 'common faint' (vasovagal syncope) and carotid sinus hypersensitivity (especially in the elderly). Orthostatic intolerance without orthostatic hypotension is increasingly recognised as due to an autonomic disturbance. New techniques are helping to unravel the functional anatomy of cerebral autonomic centres and their pathways in the causation of orthostatic intolerance.

Autonomic Nervous System↗
PubMed1998

Identification of cardiovascular pathways in the sympathetic nervous system.

1. Sympathetic autonomic neurons show distinct patterns of expression of a range of neurochemicals that can be detected immunohistochemically. Often, functionally homologous neurons in the autonomic nervous system express identical combinations of substances that serve as a chemical code that allows them to be identified among other autonomic neurons. 2. In the rat stellate ganglion, where many neurons express either immunoreactivity (IR) to neuropeptide Y (NPY) or the calcium-binding protein calbindin, a population of large post-ganglionic neurons found along the medical border of the stellate ganglion, around the origin of the cardiac nerves, expressed intense IR to both substances at all ages examined, from early postnatal to adult. 3. In the heart, in the first few postnatal weeks, many nerve terminals were IR for both NPY and calbindin, but, with increasing age, calbindin-IR was progressively lost from NPY-IR terminals. Nerve terminals IR for both calbindin and NPY were not seen around pulmonary blood vessels or in the trachea or the thymus. 4. Nerve terminals IR for calretinin, another calcium-binding protein, were present in dense pericellular baskets around neurons in the stellate IR for both calbindin and NPY. The terminals also contained nitric oxide synthase (NOS)-IR. 5. It is suggested that the calbindin- and NPY-IR neurons in the stellate ganglion are the post-ganglionic neurons that innervate the heart and that the nerve terminal containing calretinin and NOS-IR that surround them are the cardiac preganglionic terminals. It thus appears possible, in the rat, to identify the sympathetic cardiac pathway arising in the spinal cord and controlling the heart purely on the basis of chemical coding.

Animals↗
PubMed1976

Termination in the stellate ganglion of axons arising from the hilar vegetative plexus of the lung. Peripheral reflex arcs.

In cats the right lung was removed by thoracotomy. After 24-48 h the right stellate ganglion, the communicating branches between the right stellate ganglion and the right vagus, as well as the portion of both vagus nerves below and above the communicating branches, were processed for electron-microscopic investigation. Degeneration of synaptic axon terminals in the anteromedial part of the stellate ganglia, occurring after removal of the ipsilateral lung, shows that processes of ganglion cells located in the terminal ganglia of the bronchial tree establish synapses in the stellate ganglia. These results speak in favour of the existence of peripheral reflex arcs in the autonomic nervous system. For the time being, the data are not sufficient to define a new pathway related to the autonomic ganglia.

Animals↗
PubMed1995

Responses of locus coeruleus neurons to caloric stimulation in rats.

We examined the effects of caloric stimulation on the neuronal activity of the locus coeruleus (LC) and of the vestibular nucleus complex (VNC) in urethan-anesthetized rats. The single unit activity of neurons in the LC and VNC was extracellularly recorded. A polyethylene tube for caloric stimulation was inserted into the middle ear cavity on the ipsilateral side. Through the tube, the middle ear was irrigated by hot (44 degrees C), cold (30 degrees C), and ice (4 degrees C) water. The majority of neurons in the VNC showed excitation by middle ear irrigation with hot water and inhibition by ice-water irrigation. The responses occurred during caloric stimulation and disappeared immediately after the cessation of the stimulation. The results suggest that the responses of VNC neurons to caloric stimulation directly reflect changes in primary vestibular afferent activity. On the other hand, the predominant effect of caloric stimulation with hot and cold water on LC neuronal activity was inhibitory. The suppression of LC neuronal activity occurred approximately 1 min after the cessation of the caloric stimulation and persisted for 3-5 min. The results suggest that LC neurons receive processed vestibular signals. Motion sickness and vestibular dysfunction induced by caloric stimulation cause emesis, which is known as vestibulo-autonomic response. The vestibulo-autonomic syndrome can be prevented by amphetamine, a noradrenaline releaser. Therefore, the inhibitory response of noradrenergic LC neurons to vestibular stimulation may be involved in the vestibulo-autonomic response.

Afferent Pathways↗
PubMed2007

A report of cranial autonomic symptoms in migraineurs.

The presence of cranial autonomic symptoms in migraine is well known and thought to represent activation of the trigeminal parasympathetic reflex pathway similar to trigeminal autonomic cephalalgias. However, studies regarding the prevalence of these symptoms are few. The characteristics of migraineurs with cranial autonomic symptoms and the association of cranial autonomic symptoms with laterality of headache have never been studied in a clinic population. Seventy-eight consecutive subjects with migraine were recruited from the Headache Clinic of the Department of Psychiatry after exclusion of subjects with secondary headache. Their demographic data and detailed history of headache were noted and leading questions were asked regarding cranial autonomic symptoms. chi(2) test and Fisher's exact test was used for categorical variables, whereas an independent sample t-test was applied on numerical data. Spearman's correlation was used for correlational analysis of categorical variables. Female subjects (78.2%) outnumbered males and the average duration of illness in the whole sample was 3.81 years. Migraine without aura (53.8%) was the commonest diagnosis, followed by migraine with aura (24.4%). Cranial autonomic symptoms were present in 73.1% of subjects and, commonly, they were ipsilateral to headache. Moreover, strictly unilateral cranial autonomic symptoms were reported by only 32% of patients. The anatomical side of headache did not affect the presence of autonomic symptoms. Those with or without autonomic symptoms did not differ with respect to gender, diagnosis, laterality of headache or associated symptoms except phonophobia, which was more common in subjects with autonomic symptoms (P = 0.05). Those with autonomic symptoms had longer duration of illness (P = 0.03) and longer headache episodes (P = 0.04). In addition, sleep was ineffective in relieving their headache (P = 0.02). Cranial autonomic symptoms are frequent in migraineurs and are common in subjects with long duration of illness and longer headache episodes. Clinical evidence in the present study suggests that subjects with cranial autonomic symptoms have a hyperactive efferent arm of trigeminal autonomic reflex. The connections of trigeminal nucleus with the locus coeruleus and dorsal raphe nucleus may account for the observed phenotypic differences between the two groups. Further research, however, is required to elucidate the underlying neural mechanisms of cranial autonomic symptoms in migraine.

Adult↗
PubMed1993

Physiological aspects of autonomic nervous system function.

Investigations continue into the central neuronal circuitry involved in cardiovascular control, the activity of sympathetic efferents, cardiovascular responses, and experimental hypertension. Neurons within the ventrolateral medulla are integral to several reflex pathways. The activation of neurons within the A5 cell group can generate complex patterns of sympathetic and cardiovascular response. The type of respiratory modulation of a sympathetic neuron may be associated with its function. Opioid mechanisms within the central nervous system are important in cardiovascular responses to hemorrhage. The central actions of angiotensin II and atrial natriuretic peptide may blunt the baroreceptor reflex in spontaneously hypertensive rats.

Afferent Pathways↗
PubMed1999

FOS induction in brain associated with seizure and sustained cortical vasodilation in anesthetized rat.

PURPOSE: By estimating the anatomical distribution of neurons expressing c-fos protein, we sought to establish whether the intrinsic neural systems known to be implicated in the cerebrovascular regulation were activated during the increase in cortical blood flow associated with epileptic seizures. METHODS: A single unilateral microinjection of the cholinergic agonist, carbachol, in the thalamic generalized convulsive seizure area was used in anesthetized rats to elicit recurrent episodes of electrocortical epileptiform activity and an increase in cortical blood flow. Neuronal expression of Fos protein was analyzed to identify activated brain regions. RESULTS: We identified two cortical vasodilatory responses: a sustained cortical vasodilatory response associated with the continuous low-frequency, high-amplitude spiking and a transient cortical vasodilatory response invariably related to the recurrent spike-burst activity. The sustained cortical blood flow began to increase at 55-65 min, remaining significantly (p < 0.05) increased and reaching at the end of the experiment < or =182+/-17% of the prestimulated control. The electrocortical epileptic activity and the cerebral cortical vasodilation were associated with a marked increase in Fos immunoreactivity in the entorhinal and piriform cortices, the dentate gyrus, the hippocampus, and the amygdala. Fos-positive neurons also were found in specific thalamic nuclei, the cerebral cortex, the caudate-putamen, the hypothalamus, the pontine parabrachial nuclei, the dorsal raphe, and the rostral ventrolateral medulla. CONCLUSIONS: These results provide evidence that convulsive seizures elicited by cholinergic stimulation of the thalamus, in addition to limbic and somatic motor systems, activate central autonomic nuclei and their pathways, including those implicated in cerebrovascular regulation.

Animals↗
PubMed1997

NMDA receptors contribute to primary visceral afferent transmission in the nucleus of the solitary tract.

The nucleus of the solitary tract (NTS) is a principal site for coordinating the reflex control of autonomic function. The nucleus receives and organizes primary visceral (sensory) afferent inputs from the great vessels, heart, lung, and gastrointestinal organs. Glutamate, the excitatory neurotransmitter released by the primary afferent fibers, activates non-N-methyl-D-aspartate (non-NMDA) receptors on second-order neurons in the NTS. Still in question is whether NMDA receptors on the second-order neurons are also activated. Accordingly, the purpose of this study was to directly determine whether NMDA receptors contribute to synaptic transmission of primary visceral afferent input to second-order neurons in the NTS. Whole cell patch-clamp recordings were obtained from intermediate and caudal NTS neurons in rat coronal medullary slices. Excitatory postsynaptic currents (EPSCs) were evoked by stimulation of the solitary tract (1-25 V, 0.1 ms, 0.2 or 0.5 Hz) at membrane potentials ranging from -90 to +60 mV. In 28 of 32 neurons in which current-voltage relationships were obtained for solitary-tract-evoked EPSCs, the currents had short onset latencies (3.42 +/- 1.03 ms, mean +/- SD), indicating that they were the result of monosynaptic activation of second-order neurons. Solitary-tract-evoked EPSCs had both a fast and a slow component. The amplitude of the slow component was nonlinearly related to voltage (being revealed only at membrane potentials positive to -45 mV), blocked by the NMDA receptor antagonist DL-2-amino-5-monophosphovaleric acid (APV, 50 microM; n = 12; P = 0.0001), and enhanced in nominally Mg2+-free perfusate at membrane potentials negative to -45 mV (n = 5; P = 0.016), demonstrating that the slow component was mediated by NMDA receptors. The amplitude of the fast component was linearly related to voltage and blocked by the non-NMDA receptor antagonist 2,3-dihydroxy-6-nitro-7-sulfamoylbenzo(F)quinoxaline (NBQX, 3 microM; n = 9; P = 0.0014), demonstrating that the fast component was mediated by non-NMDA receptors. The slow component of the EPSCs was not blocked by NBQX (n = 6; P = 0.134), nor was the fast component blocked by APV (n = 12; P = 0.124). These results show that both NMDA and non-NMDA receptors coexist on the same second-order NTS neurons and mediate primary visceral afferent transmission in the NTS. The participation of NMDA receptors suggests that second-order neurons in the NTS may have previously unrecognized integrative capabilities in the reflex control of autonomic function.

Afferent Pathways↗
PubMed1975

Spinal autonomic afferents in elicitation of tachycardia in volume infusion in the dog.

Intravenous infusion of blood (36 ml/kg body wt) elicited tachycardia in artificially ventilated anesthetized dogs with intact autonomic innervation and in dogs with cardiac beta-receptor blockade. In contrast, infusion elicited bradycardia in dogs with section of the spinal cord at C6-C7, and in dogs with combined spinal section and cardiac beta-receptor blockade. The control heart rate was less than or equal to 110 beats/min in all the animals. The presence of infusion-induced tachycardia in dogs with beta-receptor blockade, i.e., dogs in which cardiac sympathetic efferents were blocked, and its absence in dogs with combined spinal section and beta-receptor blockade, i.e., dogs in which spinal autonomic afferents plus cardiac sympathetic efferents were blocked, may be the result of an additional interruption of spinal autonomic afferents by spinal section. It is concluded that tachycardia elicited by infusion may be partly due to a reflex with its afferent pathway in the spinal cord and its efferent pathway in the vagus nerves.

Afferent Pathways↗
PubMed1994

Diagonal ventral forebrain continuum has overlapping telencephalic inputs and brainstem outputs which may represent loci for limbic/autonomic integration.

Growing evidence indicates that three areas within the mammalian basal forebrain share many common features. Based on the similarity of connections and their adjacent spacial proximity, three forebrain nuclei are referred to as a continuum. The components of this diagonal ventral forebrain continuum (DVFC) are the central nucleus of the amygdala, the sublenticular portion of the substantia innominata, and the lateral bed nucleus of the stria terminalis. A primary concern and terminal goal of this study is to determine whether the region of this continuum which projects to the brainstem autonomic nuclei such as the vagal nuclei or the parabrachial nuclei also receives inputs from the basolateral amygdala. The first phase of this study involved determining what autonomic regions receive projections from the basal forebrain. The vagal complex and the parabrachial nuclei were found to receive the densest inputs from the DVFC. The topographic distribution of the respective retrogradely labeled cells and their collateral status is described. The second phase involved looking at afferent inputs from brainstem nuclei. The parabrachial nucleus sends reciprocal projections back to the continuum, which generally overlap the neurons which project back to the brainstem visceral nuclei. The third phase of the study indicated that the cells of the basolateral amygdala contribute a major terminal field which overlaps those cells of the basal forebrain continuum which in turn project to either the nucleus of the solitary tract or the parabrachial nucleus. The possibility that the circuits implied in this study represent the neural circuitry whereby emotional stimuli result in changes in visceral activity is addressed.

Afferent Pathways↗