[Origin and therapy of functional disorders of the autonomic nervous system].
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The Valsalva maneuver is a frequently used physiological test in evaluating the cardiovascular autonomic functions in human. Although a large pool of experimental data has provided substantial insights into different aspects of the mechanisms underlying the cardiovascular regulations during the Valsalva maneuver, so far a complete comprehension of these mechanisms and the interactions among them is unavailable. In the present study, a computational model of the cardiovascular system (CVS) and its interaction with the autonomic nervous system (ANS) was developed for the purpose of quantifying the individual roles of the CVS and the ANS in the hemodynamic regulations during the Valsalva maneuver. A detailed computational compartmental parameter model of the global CVS, a system of mathematical equations representing the autonomic nervous reflex regulatory functions, and an empirical cerebral autoregulation (CA) model formed the main body of the present model. Based on simulations of the Valsalva maneuvers at several typical postures, it was demonstrated that hemodynamic responses to the maneuver were not only determined by the ANS-mediated cardiovascular regulations, but also significantly affected by the postural-change-induced hemodynamic alterations preceding the maneuver. Moreover, the large-magnitude overshoot in cerebral perfusion immediately after the Valsalva maneuver was found to result from a combined effect of the circulatory autonomic functions, the CA, and the cerebral venous blood pressure.
Diseases of the circulatory system together with neoplastic diseases are recognised as the major health problem in the contemporary world. Their origin and aggravation may be related to the exposure to electromagnetic fields (EMFs) since theoretically, disorders in the functioning of the circulatory system are most likely due to electric impulses generated in it by external magnetic fields. The nervous system, including its autonomic part which regulates, among others, the functioning of the circulatory system, because of its electric nature is another system which may be disturbed by EMFs. From the 1960s, biological studies on the effects of power-line frequency EMFs have been carried out in many countries. In view of the applied study model, four main directions of these studies can be identified: in vitro and in vivo animal experiments, experimental studies on humans, clinical and epidemiological studies. Experimental studies on animals and humans have yielded ambiguous and very often contradictory results. Some of them indicate that EMF contributes to slowing down the cardiac rhythm and the stroke volume of the left ventricle, other results suggest their acceleration, and still other show no differences. The results of clinical studies performed in many countries in different groups of workers exposed to power-line frequency EMFs have not produced the evidence for drawing unequivocal conclusions. Again some studies reveal that those exposed show disorders in neurovegetative and blood pressure regulations (hypotension or hypertension) as well as in cardiac rhythm (bradycardia or tachycardia). Other studies do not confirm harmful effect of EMF on the circulatory system. Therefore, it is not feasible to find out, on the basis of these studies, whether and how chronic exposure to power-line frequency EMFs influences the functioning of the circulatory system, the more so as ECG standard recording has been to date the only diagnostic method, and according to the present state of knowledge it is not sufficient to assess the functioning of the circulatory system. Epidemiological studies play the most important role in the evaluation of health effects of the exposure to power-line frequency EMFs. These studies have been carried out for fifteen years, however, they do not consider the effect of chronic exposure to EMF of 50 Hz frequency on the circulatory system.
This review examines the role of the autonomic nervous system in the regulation of the immune system to understand the alteration of immunological parameters under the influence of stressors and exercise. Sympathetic innervation in secondary lymphoid organs plays a major role in immune regulation. Catecholamine released from the nerve terminal serves as the major mediator when bound to adrenergic receptors present on immunocompetent cells. Experiments using chemical and surgical denervation, catecholamine knock-out mice, and receptor antagonist and agonists revealed several important points. Sympathetic nerve activity is generally suppressive for the immunocompetent cells in the blood stream except neutrophils. Sympathetic activity facilitates detachment of T cells and NK cells from blood vessels without affecting functional adhesion molecule expression. Th1 cells express more beta 2 adrenergic receptors than Th2 cells, indicating a greater influence of sympathetic activity on Th1 response. Sympathetic action was also shown to regulate the production of chemokines. Taken together, the sympathetic nervous system does not simply suppress the immune system but might help organize the immune response sequentially and spatially by modulating the distribution of immunocompetent cells.
Four autonomic nervous system (ANS) variables: skin potential and resistance, skin blood flow and temperature - plus instantaneous heart rate and respiratory frequency - were simultaneously recorded during sporting competitions. The performances of 15 marksmen and 7 archers were analysed by comparing the variations in the six parameters during a concentration phase prior to shooting and during the shooting (or active) phase proper. The results of the performances distinguished two groups of sportsmen: firstly, the best shots and secondly, the worst shots. Comparison of the autonomic responses between the groups showed statistically significant correlations among the ANS variables. This made possible a relationship between performance characteristics and a percepto-effector factor to be defined. More precisely, this factor was defined as the number of correlations of the measured variables in the two phases, concentration and shooting. A positive relationship was demonstrated--the higher the factor, the better the performance. In addition, the stability of the factor was greater within the best marksmen and archers group. A model of the temporal change of the percepto-effector factor in both groups was given in three dimensions. This modelling of performance characteristics gave a visual indication of the differences between best/worst performances.
In the autonomic nervous system efferent signals are relayed in sympathetic and parasympathetic ganglia. Fast synaptic transmission between pre- and postsynaptic neurons is achieved by neuronal nicotinic acetylcholine receptors (nAChRs). There is still little known about the subunit composition of these receptors. Establishing the subunit composition of native neuronal nAChRs is important for the understanding of their functional properties both in vivo and after expression in heterologous expression systems. We have combined in situ hybridization and autoradiography to detect the presence of mRNAs encoding subunits of neuronal nAChRs in sympathetic and parasympathetic ganglia. Inspection of the autoradiographs showed that the hybridization signal of five riboprobes (alpha 3, alpha 4-1, alpha 7, beta 2 and beta 4) was significantly higher than the unspecific signal obtained with sense riboprobes. The distribution of alpha 7 was tissue-dependent: alpha 7 riboprobe binding was detected in the neurons of the superior cervical ganglion, adrenal medulla and ciliary ganglion. In contrast, the alpha 7 hybridization signal was found only in a small fraction (1-3%) of the neurons of the sphenopalatine and otic ganglia. Our results are consistent with the idea that alpha 3 mRNA expression levels are somewhat higher than those of alpha 7, alpha 4-1, beta 2 and beta 4.
Mammalian autonomic nervous system (ANS) development requires the combinatorial action of a number of transcription factors, which include Mash 1, Phox 2b, and GATA 3. Here we show that the bHLH transcription factor, Hand 2 (dHAND), is expressed concurrently with Mash 1 during sympathetic nervous system (SNS) development and that the expression of Hand 2 is not dependent on Mash 1. This suggests that these two bHLH factors work in parallel during SNS development. We also show that ectopic expression of Hand 2 activates the neuronal program and promotes the acquisition of a phenotype corresponding to peripheral neurons including neurons of the SNS lineage in P19 embryonic carcinoma cells. We propose that Hand 2 works in parallel with other members of the transcriptional network to regulate ANS developmental but can ectopically activate the program by a cross-regulatory mechanism that includes the activation of Mash 1. We show that this function is dependent on its interaction with the histone acetyltransferase p300/CBP, indicating that Hand 2 functions to promote ANS development as part of a larger transcriptional complex.
The concept of the APUD system and the APUDomas associated with it has evolved significantly since Pearse's description in the 1960s. Part of this evolution has been an understanding of the relationships between the APUD system and the central and autonomic nervous systems. The APUD system now referred to as the diffuse neuroendocrine system, can be linked to the central nervous system and autonomic nervous system by genetics, embryology, cellular characteristics, anatomy, interaction of the systems, and the immune system. Awareness of these relationships may enable clinicians to better understand APUDomas and lead to better methods of detection of these tumours and their treatment.
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Tests of autonomic function for the clinical autonomic neurophysiology laboratory should be noninvasive, sensitive, specific, reproducible, physiologically and clinically relevant, and not be excessively time-consuming. Laboratory evaluation is strongly indicated when the following are suspected: (1) generalized autonomic failure, (2) benign autonomic disorders that mimic life-threatening disorders, (3) distal small-fiber neuropathy, (4) the autonomic neuropathies, (5) sympathetically maintained pain, and (6) the postural orthostatic tachycardia syndrome. The preparation of the subject is important. Recommended tests should evaluate an adequate number of relevant autonomic systems. The Mayo laboratory utilizes two test batteries, the autonomic reflex screen and the reflex sympathetic dystrophy (RSD) screen. The former comprises the quantitative sudomotor axon reflex test (QSART), orthostatic blood pressure (BP) and heart rate (HR) responses to tilt, HR response to deep breathing, the Valsalva ratio, and beat-to-beat BP responses to the Valsalva maneuver, tilt, and deep breathing. The RSD screen comprises the recording of skin temperature, resting sweat output, and QSART distributions bilaterally.
Patients with diffuse toxic goiter and those with vegetative dystonia and paroxysmal permanent disorders are shown to have parasympathetic deficiency and moderate sympathetic insufficiency. In toxic goiter patients hyperhydrosis was accompanied by normal conduction along the vegetative perspiration fibers and a significant increase in foot potential amplitude. In patients having vegetative crises there was reduced conduction along the perspiration fibers. Clinical symptoms of enhanced sympathetic activity in both the diseases can be explained by weak parasympathetic influences and hypersensitivity of peripheral tissues to catecholamines. Spilberger test ascertained high reactive and personal anxiety in both groups. By modified MMPI, toxic goiter patients are characterized by hypochondriac, depressive and anxiety trends. Patients with vegetative crises were prone to demonstrative reactions, hypochondria and anxiety.
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The autonomic nervous system (ANS) plays a complex and vital role in involuntary homeostasis of bodily function. This paper discusses the function and dysfunction of the ANS in common pediatric paroxysmal disorders including epilepsy, breath-holding spells, and syncope.
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The general pharmacological properties of a novel cholecystokinin-A antagonist, loxiglumide ((+/-)-4-(3,4-dichlorobenzamido)-N-(3-methoxypropyl)-N-pentylgl utaramic acid, CR 1505, CAS 107097-80-3) on central nervous system, autonomic nervous system, cardio-respiratory system, gastrointestinal system, hematological and miscellaneous systems were investigated in experimental animals. 1. Central nervous system: At a dose of 30 mg/kg, i.v. loxiglumide showed ptosis in one of 6 mice, but at doses of 3 and 10 mg/kg, i.v. no change on gross behavior in mice. Loxiglumide had no effect on locomotor activity and thiopental-induced hypnosis, anti-convulsive activity, analgesic activity in mice and rectal temperature changes in rats. 2. Autonomic nervous system: In vitro, loxiglumide at concentrations of 10(-4) and 3 x 10(-4) mol/l slightly inhibited agonist-induced contractions in the isolated guinea pig ileum and spontaneous rhythmic contractions in the isolated non-pregnant rat uterus. But loxiglumide had no effect on oxytocin-induced contraction in isolated non-pregnant rat uterus. 3. Cardio-respiratory system: Loxiglumide had no effect on heart rate and electrocardiogram in anesthetized dogs. But it slightly increased blood pressure and decreased the frequency of respirations at a dose of 30 mg/kg, i.v. Furthermore, loxiglumide slightly decreased femoral arterial blood flow at doses of more than 3 mg/kg, i.v. On the other hand, it had no effect on contractile force or contraction rate in the isolated guinea pig atrium and resting tension in the isolated rabbit aorta. 4. Gastrointestinal system: Loxiglumide increased bile secretion at doses of 10 and 30 mg/kg, i.v. in anesthetized rats and at doses of 3, 10 and 30 mg/kg, i.v. in anesthetized dogs. However, total bile acid output was not affected by loxiglumide. On the other hand, loxiglumide had no effect on pancreatic secretion, gastric secretion and gastric emptying in rats and intestinal transport activity in mice. 5. Hematology: In vitro, in the case of samples without bovine serum albumin, at concentrations of more than 1.9 x 10(-3) mol/l loxiglumide showed hemolysis, while in the case of samples with bovine serum albumin, at concentrations of more than 6.9 x 10(-3) mol/l loxiglumide showed hemolysis, and its maximal potency was weak compared to albumin-free conditions. On the other hand, in vivo, loxiglumide had no effect on hemolysis. In addition, it had no effect on platelet aggregation, prothrombin time and activated partial thromboplastin time. 6. Miscellaneous pharmacological actions: Loxiglumide had no effect on local anesthetic activity in guinea pigs and renal function in mice. These results suggest that loxiglumide seems to produce no serious side effects on the central nervous system, autonomic nervous system, cardio-respiratory system, gastrointestinal system, hematological and miscellaneous systems at pharmacologically effective doses.
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