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PubMed1975

Minimal brain dysfunction, stimulant drugs, and autonomic nervous system activity.

Autonomic base levels and responsivity to stimuli were investigated in normal and minimally brain dysfunctioned (MBD) children. Continuous recordings of skin conductance, heart rate, skin temperature, and respiration rate were made during rest, at presentation of tones, and when performing a reaction time task. No significant differences in base levels were obtained between normal and MBD children when not taking drugs, but stimulant medication increased skin conductance and heart rate and decreased skin temperature and reaction time. The MBD children were less reactive, autonomically, to all types of stimuli. Stimulant drugs decreased electrodermal responsivity, which was predictable from concurrent changes in base line skin conductance and skintemperature. The MBD performance deficits are not related to lower autonomic responsivity or lower absolute base levels of arousal, but MBD children may perform better at relatively high autonomic base levels.

Acoustic Stimulation↗
PubMedDate not supplied

Local regulation of the immune response by the autonomic nervous system.

The autonomic innervation of the lymphoid tissue is currently visualized as a channel for neural regulation of immunity. Several reports have dealt with the alteration of antibody responses of spleen and lymph nodes following sympathectomy, and less often, parasympathectomy. This article reviews published data on the local effects of sympathetic and parasympathetic neurons innervating immunocompetent organs on immune responsiveness. A model comprising bilateral lymphoid organs (the submaxillary lymph nodes) and the local ipsilateral manipulation of their regional sympathetic nerves (derived from the superior cervical ganglia) and of their regional parasympathetic nerves (conveyed through the lingual nerve-chorda tympani) allowed the description of purely local effects of the autonomic nerves independent of the systemic effects of the surgical manipulation itself. By employing this model, the following were observed. (1) After the unilateral sympathetic denervation of murine submaxillary lymph nodes by superior cervical ganglionectomy (SCGx), ipsilateral increases in plate-forming cell (PFC) activity, delayed hypersensitivity and graft-versus-host reactions were observed as compared to the contralateral, sham-operated, submaxillary lymph nodes. During degeneration of peripheral sympathetic nerves shortly after SCGx, PFC activity in ipsilateral submaxillary lymph nodes decreased significantly. (2) The local parasympathetic decentralization of murine submaxillary lymph nodes, achieved by the unilateral section of the chorda tympani, resulted in decreases of PFC activity, when challenged 10-20 days after denervation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

[General pharmacological action of 4-(o-benzylphenoxy)-N-methylbutylamine hydrochloride (MCI-2016, bifemelane hydrochloride). Influence on respiratory and cardiovascular systems, renal function, autonomic nervous system, isolated smooth muscle and digestive organs].

MCI-2016 at 3 mg/kg, i.v., caused slight changes in systemic blood pressure (SBP), heart rate (HR), respiratory rate (RR) and ECG but at 10 mg/kg, i.v., it caused a significant increase in RR, decrease in SBP, increase or decrease in HR and a moderate change in ECG. Biphasic changes in SBP, HR and blood flow were sometimes observed after high doses. MCI-2016 also decreased SBP at 30 mg/kg, i.p., in SHR. MCI-2016 (50 mg/kg, p.o./day) showed little influence on SBP, HR and ECG in conscious beagle dogs. In isolated hearts, MCI-2016 decreased HR and contractility at the concentrations above 10(-5) g/ml, and 30 micrograms, i.a. MCI-2016 prolonged the AVCT at 10 mg/kg, i.v. MCI-2016 (i.v. or i.a.) moderately increased cerebral and femoral artery blood flows. MCI-2016 did not change CMRO2, but decreased MVO2. Coronary and renal artery flows were moderately increased by 10 mg/kg, i.v., of MCI-2016. Renal function was suppressed after 10 mg/kg, i.v., or 300 mg/kg, p.o., of MCI-2016. MCI-2016 potentiated the action of NE (increase in SBP, contractions of nictitating membrane and vas deferens), but showed little anti-cholinergic action. In contrast, MCI-2016 moderately increased gastrointestinal motility and salivatory response. As for the influence on isolated smooth muscles, MCI-2016 antagonized the contraction of blood vessels by high K+ at 10(-6) g/ml, or more, and it depressed the contractions by ACh, 5-HT, histamine and BaCl2 and also depressed spontaneous movements of uterus and ileum at 10(-5) M or more, in a nonspecific manner. MCI-2016 had no influence on liver damage and bile secretion, but inhibited stress ulcer and gastric acid secretion on the one hand, and caused gastric damage (125 mg/kg p.o., or more) on the other hand.

Animals↗
PubMed1986

[Effects of the autonomic nervous system in supraventricular arrhythmia].

Influences of the autonomic nervous system may cause modifications of the initiation, continuation and discontinuation of supraventricular rhythm disturbances. Whether or not clinically relevant bradycardia syndromes (such as the hypersensitive carotid sinus syndrome and the sick sinus syndrome) also may exist primarily on a functional basis, remains to be proven. Organic pathology, whether it is clinically apparent or not, probably provides the basis for the activation of influences on the autonomic nervous system. In atrial fibrillation and atrial flutter the influence of the autonomic nervous system is apparent in a form of the vagotonically and sympathotonically evoked paroxysms. In the case of persistent atrial fibrillation vagal and sympathotonically transmitted changes in the AV-dromotropy determine the mode of heart rate. Junctional re-entry tachycardias and re-entry tachycardias under the influence of accessory pathways, are potentially triggered by mechanisms, as transmitted by the autonomic nervous system. Furthermore, such autonomic influences are responsible for changes in the conducting velocity and the refractory properties, as produced by parallel conducting pathways. Hemodynamic changes themselves, which are induced at the very beginning of the tachycardia, may activate other electrophysiological mechanisms and thereby cause a modification in the type of tachycardia in question.

Arrhythmias, Cardiac↗
PubMed2003

Autonomic Nervous System Dysfunction in Parkinson's Disease.

Autonomic nervous system (ANS) dysfunction is common in Parkinson's disease (PD), affects 70% to 80% of patients, and causes significant morbidity and discomfort. Autonomic nervous system dysfunction symptoms in PD include sexual dysfunction, swallowing and gastrointestinal disorders, bowel and bladder abnormalities, sleep disturbances, and derangements of cardiovascular regulation, particularly, orthostatic hypotension. Autonomic nervous system dysfunction in PD may be caused by an underlying degenerative process that affects the autonomic ganglia, brainstem nuclei, and hypothalamic nuclei. Anti-parkinsonian medications can cause or worsen symptoms of ANS dysfunction. The care of a PD patient with ANS dysfunction relies on its recognition and directed treatment, including coordinated care between the neurologist and appropriate subspecialist. Pharmacotherapy may be useful to treat orthostasis, gastrointestinal, urinary, and sexual dysfunction.

Journal Article↗
PubMed2006

Multiple sclerosis and the autonomic nervous system.

Symptoms related to alterations of the autonomic nervous system are frequent in patients with multiple sclerosis (MS). Bladder or bowel dysfunction or impairment of sexual performance is highly distressing for most MS patients,whereas the clinical relevance of other autonomic symptoms is less clear. Cardiovascular autonomic alterations might relate to clinical signs such as orthostatic intolerance; a relationship with fatigue is uncertain. However, the frequency of abnormal findings in tests for the cardiovascular autonomic system varies due to the lack of standardized test performance or differentially used cut-off values. The incidence of additional symptoms such as pupillomotor or sweating alterations and especially their relationship to overall autonomic nervous system abnormalities is not well known. Although their impact on daily life is low, they can at least serve as diagnostic tools. Beside these clinical aspects, alterations of the autonomic nervous system have also been reported to alter immunological cascades in experimental conditions. However, corresponding results have not been confirmed in clinical trials yet.

Autonomic Nervous System↗
PubMed1995

[Function of the autonomic nervous system in uremia].

Autonomic impairement is associated with poor prognosis in many diseases. The article (first of three parts) critically reviews arguments found in the literature showing autonomic dysfunction in chronic renal failure patients. The autonomic nervous system problems will become of great clinical relevance considering increasing number and age of uremic patients being dialysed worldwide.

Animals↗
PubMed1991

Autonomic nervous system disorders in Parkinson's disease.

This paper gives a review on the clinical features of autonomic failure which occur in idiopathic Parkinson's disease (PD), mainly based on the recent publications, especially from Japan. In 1817, James Parkinson already mentioned bowel and bladder dysfunctions in his original article. Since then, a number of clinical studies have disclosed the occurrence of autonomic failure in this disease. It is known that relatively minor degrees of orthostatic hypotension are not rare, but other features of autonomic failure are rather uncommon, generally mild in severity and nonprogressive. Orthostatic hypotension is suggested as a possible side effect of L-dopa. Postprandial hypotension is occasionally found, and vasopressin is proven to prevent it remarkably. There is low electrocardiographic R-R interval variability which indicates impaired parasympathetic activity. Thermoregulatory sweating is nearly normal, but its center is functionally impaired. Resting skin temperature is slightly lower. Both salivation and lacrymation are quantitatively within normal limits. Little is known on sexual function in PD.

Animals↗
PubMed1994

[Diabetes, obesity, hypertension and the autonomic nervous system].

Functional changes of the autonomic nervous system may represent a common pathophysiologic factor in the association between non insulin-dependent diabetes, obesity, and essential hypertension. In all these conditions a number of sympathetic and/or parasympathetic dysfunctions consistent with autonomic neuropathy or simply with functional adaptations to haemodynamic changes have been reported. Autonomic neuropathy is a well known diabetic complication which is responsible for some clinical aspects of different severity. Subtle sympathetic and parasympathetic abnormalities possibly affecting thermogenesis have been shown in obese people. An increased sympathetic activity has been proposed as one of the pathogenetic mechanisms of essential hypertension. Finally, the association between diabetes, obesity, hypertension and sympathetic overactivity could be explained by a common trans-membrane ionic disturbance with an increase of intracellular calcium and a decrease of both intracellular magnesium and pH.

Autonomic Nervous System↗
PubMed1987

Localization of autonomic nervous system dysfunction in dialysis patients.

Autonomic nervous system dysfunction has been described frequently in uremic patients. The purpose of this study is to determine the localization of this abnormality and to study the possible relationship between autonomic dysfunction and the occurrence of dialysis hypotension. Sixteen consecutive patients participated in the study, 5 of whom had a history of dialysis-induced hypotension. These 5 patients were compared to the other 11 as regards the cardiovascular response to isoproterenol infusion, tilt test and arteriovenous (AV) fistula occlusion. None of the responses to the above mentioned stimuli was significantly different between the 2 groups. In the whole study population, an index of parasympathetic control of heart rate (variation of heart period, VHP) was reduced (31 +/- 5 vs. 59 +/- 9 ms in age-matched controls; p less than 0.025). Heart rate and diastolic blood pressure response to isoproterenol infusion was normal (+23 +/- 2 beats/min and -9 +/- 3 mm Hg; p less than 0.005 for both), indicating normal response of effector organs to beta-adrenergic agonist stimulation. Similarly, plasma norepinephrine increased significantly (+294 +/- 51 pg/ml; p = NS from normal laboratory values) in response to head-up tilt, and heart rate increased simultaneously in all but 5 patients. Blood pressure response was within normal after 10 min of head-up tilt at 60 degrees in all but 3 patients; only 1 of these 3 patients was in the group of dialysis hypotension. However, during AV fistula occlusion, heart rate did not change markedly, despite the significant increase in systolic blood pressure, suggesting an altered sensitivity of baroreceptor reflex arc.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

[Neuropathological background of spinocerebellar degeneration--with special reference to autonomic nervous system lesions in olivopontocerebellar atrophy, Shy-Drager syndrome and multiple system atrophy].

For elucidation of actual status of olivopontocerebellar atrophy (OPCA) in nosological relation to Shy-Drager syndrome (SDS) and multiple system atrophy (MSA), neuropathological examination with morphometric survey on the intermediolateral column of the spinal cord was performed. The materials were 13 cases registered in our laboratory. Clinically, they consisted of 9 sporadic OPCA including 2 cases with prominent autonomic failure, and 4 hereditary spinocerebellar degeneration. In the autonomic nervous system of CNS, degeneration of the intermediolateral column was found in the sporadic cases without exception, irrespective of presence or absence of orthostatic hypotension, while the hereditary cases showed neither orthostatic hypotension nor neuronal loss in the nucleus. The autonomic centers in the brain-stem and cerebellum were systematically affected in both the sporadic and the hereditary cases. It was particularly remarked that the fastigial nucleus, tractus and nucleus solitarius, which have been suggested to be related to cardiovascular control, was severely affected. The locus coeruleus, on the other hand, was less severely affected in the hereditary cases. The most remarkable finding was that there was no case with neuropathological change restricted only to the olivo-ponto-cerebellar (OPC) and/or autonomic nervous systems. The sporadic cases had OPC system degeneration with striato-nigral degeneration (SND) and autonomic nervous system degenerations, irrespective of differences in clinical features from case to case. It should be emphasized that the actual neuropathological status of our sporadic cases could be regarded as a multisystemic degeneration inevitably combined with OPC system degeneration, apart from whether such cases are designated as MSA or not. Finally it was remarked that the hereditary cases were different from the sporadic cases in that there occurred far less severe involvement of the locus coeruleus and intermediolateral column, and primary degeneration of the substantia nigra different obviously from SND.

Adult↗
PubMed2004

[Autonomic nervous system in heart failure].

The autonomic nervous system (ANS), a complex and self-organized entity, plays a crucial role in cardiovascular regulation. In this review, the authors describe some concepts of anatomo-physiology and cellular/molecular biology of the ANS and of its two major components, the parasympathetic and sympathetic system, both in the normal individual and in the patient with heart failure. Adrenergic and cholinergic neurotransmission, neurotransmitters, adrenergic and cholinergic receptors and intracellular signal transduction are discussed. Some aspects of sympathetic-parasympathetic interaction at the cellular level are described as well as the opposite role of two cyclic nucleotides, cyclic adenosine and guanosine monophosphate. Major emphasis is placed on the beta-adrenergic system, the combination of the beta receptor, G protein complex and adenylyl cyclase. The activation of neurohumoral compensatory mechanisms in heart failure is discussed as well as the increasingly recognized importance of sympathetic overactivation and parasympathetic tonus reducting in this setting. Cellular mechanisms of adrenergic stimulation in heart failure and its consequences are presented, with special focus on down-regulation of beta-1 adrenergic receptors; the authors analyze the steps of phosphorlation and oncoupling, sequestration, internalization and lysosomal degradation, the main result of which is reduced response to catecholamines.

Autonomic Nervous System↗
PubMed1991

Orthostatic hypotension in human immunodeficiency virus infection may be the result of generalized autonomic nervous system dysfunction.

We used an autonomic nervous system (ANS) testing battery to determine if generalized ANS dysfunction was present in five human immunodeficiency virus-positive (HIV+) patients presenting with severe orthostatic hypotension (OH). All five patients had abnormal ANS testing, which demonstrated both sympathetic and parasympathetic defects, i.e., generalized ANS dysfunction. Treatment with fludrocortisone effectively reversed the OH in four of the five patients. The OH was transient in these four patients. We believe it is important to recognize that OH may be the result of generalized ANS dysfunction in HIV-positive patients and that it can be effectively treated.

Autonomic Nervous System↗