Showing papers on "Autonomic nervous system published in 1994"

Human Embryology and Developmental Biology

Abstract: Carnegie Stages of Early Human Embryonic Development (Weeks 1-8) Major Developmental Events During the Fetal Period Part I: Early Development and the Fetal-Maternal Relationship Chapter 1: Getting Ready for Pregnancy Gametogenesis Preparation of the Female Reproductive Tract For Pregnancy Hormonal Interactions Involved with Reproduction in Males Chapter 2: Transport of Gametes and Fertilization Ovulation and Egg and Sperm Transport Fertilization Chapter 3: Cleavage and Implantation Cleavage Embryo Transport and Implantation Chapter 4: Molecular Basis for Embryonic Development Fundamental Molecular Processes in Development Chapter 5: Formation of Germ Layers and Early Derivatives Two-Germ-Layer Stage Gastrulation and the Three Embryonic Germ Layers Induction of the Nervous System Cell Adhesion Molecules Chapter 6: Establishment of the Basic Embryonic Body Plan Development of the Ectodermal Germ Layer Development of the Mesodermal Germ Layer Development of the Endodermal Germ Layer Basic Structure of the 4-Week Old Embryo Chapter 7: Placenta and Extraembryonic Membranes Extraembryonic Tissues Chorion and Placenta Placenta After Birth Placenta and Membranes in Multiple Pregnancies Chapter 8: Developmental Disorders: Causes, Mechanisms, and Patterns General Principles Causes of Malformations Developmental Disturbances Resulting in Malformations Part II: Development of the Body Systems Chapter 9: Integumentary, Skeletal and Muscular Systems Integumentary System Skeleton Muscular System Chapter 10: Limb Development Initiation of Limb Development Regulative Properties and Axial Determination Outgrowth of the Limb Bud Morphogenetic Control of Early Limb Development Development of Limb Tissues Chapter 11: Nervous System Establishment of the Nervous System Early Shaping of the Nervous System Histogenesis Within the Central Nervous System Craniocaudal Pattern Formation and Segmentation Peripheral Nervous System Autonomic Nervous System Later Structural Changes in the Central Nervous System Ventricles, Meninges, and Cerebrospinal Fluid Formation Cranial Nerves Development of Neural Function Chapter 12: Neural Crest Origins of the Neural Crest Migrations of the Neural Crest Differentiation of Neural Crest Cells Major Divisions of the Neural Crest Trunk Neural Crest Circumpharyngeal Neural Crest Cranial Neural Crest Chapter 13: Sense Organs Eye Ear Chapter 14: Head and Neck Early Development of the Head and Neck Fundamental Organization of the Pharyngeal Region Development of the Facial Region Development of the Pharynx and Its Derivatives Chapter 15: Digestive and Respiratory Systems and Body Cavities Digestive System Respiratory System Body Cavities Chapter 16: Urogenital System Urinary System Genital System Sexual Duct System External Genitalia Chapter 17: Cardiovascular System Developmental of the Vascular System Developmental and Partitioning of the Heart Initiation of Cardiac Function Fetal Circulation Chapter 18: Fetal Period and Birth Growth and Form of the Fetus Fetal Physiology Parturition Adaptations to Postnatal Life Overview Answers to Clinical Vignettes and Review Questions

Autonomic cardiac control. III. Psychological stress and cardiac response in autonomic space as revealed by pharmacological blockades.

Abstract: Behavioral contexts can evoke a variety of autonomic modes of response, characterized by reciprocal, coactive, or independent changes in the autonomic divisions. In the present study, we investigated the reactive autonomic control of the heart in response to psychological stressors, using quantitative methods for analyzing single and double autonomic blockades, and through the use of noninvasive indices based on heart period variability and systolic time intervals. Analysis of the effects of pharmacological blockades revealed an overall pattern of increased sympathetic and decreased parasympathetic control of the heart during speech stress, mental arithmetic, and a reaction-time task. Unlike the classical reciprocal sympathetic-parasympathetic response to orthostatic challenge, however, the responses of the autonomic branches to stress were uncorrelated. This reflected notable individual differences in the mode of autonomic response to stress, which had considerable stability across stress tasks. The putative noninvasive indices of sympathetic (preejection period) and parasympathetic (respiratory sinus arrhythmia) control changed in accord with the results of pharmacological blockades. Together, these results emphasize the substantial individual differences in the mode of autonomic response to stress, the advantages of a quantitative approach to analyzing blockade data, and the importance of validity estimates of blockade data.

Social neuroscience: Autonomic, neuroendocrine, and immune responses to stress

Abstract: The immune system is influenced by central nervous system processes that are shaped by social and psychological factors. Considerations of social factors, intrapersonal processes, and autonomic psychophysiology therefore may contribute to a fuller understanding of both immune and brain function. Research reviewed here (a) examines the socioemotional factors that contribute to, or moderate, responses to brief and chronic stressors, (b) determines whether or not stable individual differences in heart rate reactivity predict neuroendocrine and immune responses to a brief psychological stressor and to an influenza virus vaccine, and (c) investigates the autonomic origins of individual differences in low and high heart rate reactivity and their relationship to neuroendocrine and immune responses to chronic and acute stressors. Among our findings are: (a) acute psychological stressors activate the sympathetic adrenomedullary system across individuals and affect immune function; and (b) individuals characterized by high sympathetic cardiac reactivity to acute psychological stressors also show a relative activation of the hypothalamic pituitary adrenocortical system and altered immune function.

p75-deficient embryonic dorsal root sensory and neonatal sympathetic neurons display a decreased sensitivity to NGF

Abstract: To understand the role of low-affinity neurotrophin receptor p75 in neural development, we previously generated mice carrying a null mutation in the p75 locus (Lee, K. F., Li, E., Huber, L. J., Landis, S. C., Sharpe, A. H., Chao, M. V. and Jaenisch, R. (1992) Cell 69, 737–749). To elucidate the mechanisms leading to deficits in the peripheral nervous system in p75 mutant mice, we have employed dissociated cultures to examine the responses of p75-deficient dorsal root ganglion (DRG) and superior cervical ganglion (SCG) neurons to different neurotrophins. We found that p75-deficient DRG and SCG neurons displayed a 2- to 3-fold decreased sensitivity to NGF at embryonic day 15 (E15) and postnatal day 3 (P3), respectively, ages that coincide with the peak of naturally occurring cell death. Furthermore, while p75-deficient E15 DRG neurons did not change their response specificity to BDNF, NT-3, and NT-4/5, P3 SCG neurons became more responsive to NT-3 at higher concentrations (nanomolar ranges). These results may help explain the deficits in the peripheral nervous system in p75 mutant mice and provide evidence that p75 can modulate neurotrophin sensitivity in some neurons.

Human autonomic rhythms: vagal cardiac mechanisms in tetraplegic subjects

Abstract: 1. We studied eight young men (age range: 20-37 years) with chronic, clinically complete high cervical spinal cord injuries and ten age-matched healthy men to determine how interruption of connections between the central nervous system and spinal sympathetic motoneurones affects autonomic cardiovascular control. 2. Baseline diastolic pressures and R-R intervals (heart periods) were similar in the two groups. Slopes of R-R interval responses to brief neck pressure changes were significantly lower in tetraplegic than in healthy subjects, but slopes of R-R interval responses to steady-state arterial pressure reductions and increases were comparable. Plasma noradrenaline levels did not change significantly during steady-state arterial pressure reductions in tetraplegic patients, but rose sharply in healthy subjects. The range of arterial pressure and R-R interval responses to vasoactive drugs (nitroprusside and phenylephrine) was significantly greater in tetraplegic than healthy subjects. 3. Resting R-R interval spectral power at respiratory and low frequencies was similar in the two groups. During infusions of vasoactive drugs, low-frequency R-R interval spectral power was directly proportional to arterial pressure in tetraplegic patients, but was unrelated to arterial pressure in healthy subjects. Vagolytic doses of atropine nearly abolished both low- and respiratory-frequency R-R interval spectral power in both groups. 4. Our conclusions are as follows. First, since tetraplegic patients have significant levels of low-frequency arterial pressure and R-R interval spectral power, human Mayer arterial pressure waves may result from mechanisms that do not involve stimulation of spinal sympathetic motoneurones by brainstem neurones. Second, since in tetraplegic patients, low-frequency R-R interval spectral power is proportional to arterial pressure, it is likely to be mediated by a baroreflex mechanism. Third, since low-frequency R-R interval rhythms were nearly abolished by atropine in both tetraplegic and healthy subjects, these rhythms reflect in an important way rhythmic firing of vagal cardiac motoneurones.

Growth of the rat prostate gland is facilitated by the autonomic nervous system.

Abstract: Many factors are implicated in the development of prostatic growth: androgens, growth factors, and stromo-epithelial interaction. This study examines the role of the sympathetic and parasympathetic branches of the autonomic nervous system control of different aspects of rat prostate growth and atrophy. Unilateral sympathectomy leads to decreases in ventral prostate weight, DNA, and protein content in the lesioned side. Unilateral parasympathectomy leads to increases in ventral prostate weight, DNA, and protein content in the intact side. The separate effects of sympathectomy and parasympathectomy are maintained across a diverse combination of neural manipulations. Significant re-innervation does not occur by 60 days after manipulation as assessed by tissue norepinephrine levels. There appears to be a differential effect of the autonomic nervous system on growth and maintenance of the ventral prostate. The mechanism of contralateral hyperplasia and ipsilateral atrophy has potential significance in understanding human abnormal prostate growth.

The effects of an acute psychological stressor on cardiovascular, endocrine, and cellular immune response: a prospective study of individuals high and low in heart rate reactivity

Abstract: High and low reactors were preselected on the basis of their heart rate reactivity to a speech stressor in a prescreening session. In the main study, subjects were exposed to a mental arithmetic plus noise stressor. Cardiovascular activity was recorded during baseline and stressor, and blood was drawn prior to and following the stressor for endocrine and immune assays. Results revealed that the stressor decreased the blastogenic response to concanavalin A and increased natural killer cell numbers and cytotoxicity, absolute numbers of CD8+ T-lymphocytes, norepinephrine and epinephrine levels, heart rate, and blood pressure responses. In addition, cortisol and natural killer cell cytotoxicity responses to the stressor differentiated individuals high versus low in heart rate reactivity. These results suggest that the interactions among the autonomic nervous system, endocrine system, and immune system are not only amenable to psychophysiological analysis but that such analyses may play an important role in illuminating underlying mechanisms.

Idiopathic autonomic neuropathy: Clinical, neurophysiologic, and follow-up studies on 27 patients

Abstract: We evaluated the natural history, electrophysiologic characteristics, spectrum of autonomic involvement, pathology, and laboratory features in 27 patients with idiopathic autonomic neuropathy who were followed up for a mean of 32 months. The typical features of idiopathic autonomic neuropathy include the absence of an associated disease, frequent history of preceding infection, and acute or subacute onset with a monophasic course. The spectrum of autonomic involvement ranges from panautonomic to selective adrenergic or cholinergic failure. There is infrequent involvement of somatic nerve fibers as assessed by routine nerve conduction studies. Pathologic features include the presence of a small inflammatory mononuclear cell infiltrate in the epineurium. Recovery tends to be gradual and frequently incomplete. The acute onset, frequent antecedent viral infection, selectivity of involvement by fiber type and autonomic level, and presence of perivascular mononuclear cell infiltration suggest that the underlying mechanism is likely to be immune-mediated. These observations may justify plasma exchange or other immunosuppressive modalities as early therapeutic intervention in patients with progressive disability.

Cardiovascular autonomic reflexes in brain infarction.

Abstract: Increased sympathetic activity is associated with cardiovascular complications in stroke, but the role of the parasympathetic nervous system has not been carefully outlined. In the present study our purpose was to assess quantitatively autonomic cardiovascular disturbances in brain infarction by measuring cardiovascular autonomic reflexes. We studied the autonomic regulation of cardiovascular functions prospectively in 40 patients with brain infarction (acute phase, 1 month, and 6 months) and in 55 healthy control subjects by recording heart rate and blood pressure responses to normal and deep breathing, the Valsalva maneuver, tilting, and isometric work. In the acute phase, heart rate responses to normal breathing, deep breathing, the Valsalva maneuver, and tilting were significantly (P < .05) impaired in both hemispheric and brain stem infarctions, thus indicating hypofunction of the parasympathetic nervous system. At 1 month heart rate responses to normal breathing (brain stem, P < .05), the Valsalva maneuver (brain stem, P < .01), and tilting (hemispheric, P < .05) were still significantly lower than those of the control subjects, but at 6 months significant suppression of the response was found only in tilting (hemispheric, P < .05). These findings suggest that in addition to the previously well-established sympathetic hyperfunction, brain infarction also seems to cause parasympathetic hypofunction, brain which may be involved in cardiovascular and other known manifestations of autonomic failure associated with stroke.

Autonomic reflex dysfunction in patients presenting for elective surgery is associated with hypotension after anesthesia induction

Abstract: BACKGROUND: Autonomic reflex dysfunction in patients with diabetes is associated with an increased incidence of hypotension after induction of anesthesia. Whether this finding can be extrapolated to patients with autonomic dysfunction from other causes (e.g., advanced age, hypertension, altered ventricular function) has not been established. METHODS: The authors investigated whether autonomic reflex dysfunction in a more generalized patient group (26 consecutively consenting day-surgery patients older than 39 yr) was similarly associated with the occurrence of hypotension after induction. Preoperative tests of autonomic function included: Valsalva maneuver, change in heart rate with forced breathing, change in heart rate and blood pressure with standing, and spectral analysis of heart rate variability. Anesthesia was induced with 3-5 mg/kg thiopental, 2 micrograms/kg fentanyl, and 60% N2O; 0.1 mg/kg vecuronium was used for paralysis; 0-1.5% isoflurane was added for maintenance of anesthesia after intubation. Noninvasive measurements of mean blood pressure were obtained every minute for 10 min after induction and then every 3 min until skin incision. RESULTS: Twelve patients developed hypotension (mean blood pressure < 70 mmHg), and 14 patients did not. Measurements of autonomic reflex function were significantly more abnormal in the patients who developed hypotension (P < 0.006 for Valsalva measurements, heart rate variability parameters, and change in heart rate with forced breathing). Using critical test values for autonomic tests, the incidence of hypotension was 67-83% in patients with autonomic nervous system dysfunction versus 9-17% in other patients. CONCLUSIONS: The results document that: (1) some degree of autonomic reflex dysfunction is not uncommon in patients older than 39 yr presenting for elective surgery, and (2) such dysfunction is associated with an increased incidence of hypotension when using the described induction technique.

Sympathetic neural reactivity to stress does not increase with age in healthy humans

Abstract: Sympathetic nervous system reactivity to stress is though to increase with age in humans. We tested this hypothesis by recording postganglionic sympathetic nerve activity to skeletal muscle (MSNA) ...

Exercise and aging: autonomic control of the circulation.

Abstract: This review describes age-related changes in autonomic control of the circulation during exercise and the associated effects on exercise capacity. The increase in heart rate during exercise becomes smaller with aging probably due to both less withdrawal of cardiac vagal tone and diminished beta-adrenergic responsiveness. The latter also appears to contribute to an attenuation in the left ventricular contractile response to exercise despite greater beta-adrenergic stimulation. At rest, muscle sympathetic nerve activity and arterial plasma norepinephrine spillover rates are elevated in older humans. With aging, sympathetically mediated vasoconstriction in nonactive muscle is augmented during brief dynamic exercise. Paradoxically, during more prolonged exercise increases in plasma norepinephrine concentrations/spillover rates are not greater with age. These age-related changes do not adversely affect submaximal exercise performance at a particular % maximal oxygen consumption. However, the lower peak heart rate and attenuated left ventricular contractile response reduce maximal cardiac output, oxygen consumption, and exercise capacity. In older humans, aerobic exercise training lowers heart rate at rest, reduces levels of heart rate and plasma catecholamines at the same absolute submaximal workload, and, at least in men, improves left ventricular performance during peak exercise, but does not reduce, and may even increase, basal sympathetic nerve activity.

Increase in muscle nerve sympathetic activity in humans after food intake.

Abstract: 1. The influence of the intake of different nutrients on muscle nerve sympathetic activity was studied by use of microneurography. Muscle nerve sympathetic activity, heart rate, blood pressure and the insulin response were monitored for 90 min in 39 healthy, lean, normotensive subjects (mean age 26 years) who received 100 g of glucose in 300 ml of water (n = 8), 50 g of fat in 250 ml of water (n = 8), 100 g of lean meat corresponding to 40 g of protein with 250 ml of water (n = 8), 300 ml of water only (n = 7) or a mixed meal (1750 kJ) (n = 8). 2. All types of food evoked an increase in muscle nerve sympathetic activity whereas water caused no change. The increase in muscle nerve sympathetic activity was already significant at 15-30 min and was still strongly significant at 90 min. The effect of glucose was significantly greater than that of fat and protein; the mixed meal caused an intermediate response. Blood pressure changes were minor. 3. It is concluded that a sustained increase in muscle nerve sympathetic activity occurs regularly after any type of food intake. A rise in muscle nerve sympathetic activity takes place in the absence of an insulin response, and insulin contributes to only part of the increase after ingestion of glucose or a mixed meal. The muscle nerve sympathetic activity response is thought to be of importance for the redistribution of blood to the splanchnic region after a meal. Lack of this response is likely to explain postprandial hypotension in autonomic failure.

Identification of antibodies with muscarinic cholinergic activity in human Chagas' disease: pathological implications.

Abstract: We examined the possible role of altered humoral immunity in dysautonomic syndrome in Chagas' disease by analyzing the effect of sera and IgG on the binding of radioligand to heart muscarinic cholinergic receptors and on the contractility of myocardium. Human Chagasic IgG inhibited in a non-competitive manner the binding of [3H]quinuclidinyl benzilate to the cardiac cell membrane. Moreover, human Chagasic IgG behaved as a partial muscarinic cholinergic agonist, reducing heartcontractility and inhibiting the action of pilocarpine. The prevalence of the cholinergic antibody activity was higher in sera from T. cruzi-infected asymptomatic individuals with dysautonomic syndrome than in those without autonomic nervous system alterations. The presence of these antibodies could explain the progressive receptor blockade in the parasympathetic branch of the autonomic nervous system, leading to dysautonomia.

Joint inflammation is reduced by dorsal rhizotomy and not by sympathectomy or spinal cord transection.

Abstract: OBJECTIVES--To investigate the role of primary afferents, sympathetic postganglionic efferents and descending systems on the central control of peripheral inflammation. METHODS--Acute inflammation was induced by intra-articular injection of kaolin and carrageenan into the knee joint cavity of the rat. Before the induction of the arthritis, a unilateral dorsal rhizotomy, a chemical (phentolamine) and/or surgical sympathectomy, or a spinal transection was performed. Joint inflammation (joint circumference and thermographic readings) and behavioural signs were assessed. RESULTS--Only arthritic animals with a dorsal rhizotomy showed a significant reduction of the inflammatory response compared with control arthritic animals. No significant differences in the inflammatory response occurred following sympathectomy or spinal transection. The animals who received sympathectomy showed similar behavioural manifestations to the arthritic animals. CONCLUSIONS--The central terminals of primary afferents are important in the development of acute joint inflammation since dorsal rhizotomy attenuated the inflammatory response in the knee joint. The sympathetic nervous system is not involved in the acute inflammatory phase of this arthritis model. The central processes controlling acute inflammation involve a local spinal circuit since spinal cord transection at T9 has no effect on the inflammation.

Control of the Gastrointestinal Tract by Enteric Neurons

Abstract: The gastrointestinal (GI) tract is host to three physiological effector systems: visceral smooth muscle, which is responsible for motility; intestinal musosa, which is responsible for fluid and electrolyte homeostasis; and the vascula­ ture. The three divisions of the autonomic nervous system (sympathetic, parasympathetic, and enteric) contribute to the neural control of each of these effector systems although it seems fair to say that the enteric nervous system plays the predominant role in neuronal modulation of GI function. Complex reflex activities involving GI motility, intestinal ion transport, and mucosal blood flow occur in the absence of extrinsic autonomic and sensory input. Thus sensory, motor, and interneuronal elements mediating these types of reflex loops are contained within the two neural networks of the enteric nervous system: the myenteric (Auerbach's), and thc submucosal (Meissner's) plexus (Figure 1). The major function of myenteric neurons is to control GI motility, while the submucosal neurons are primarily involved with modulation of GI blood flow and intestinal ion transport. Modem studies concerning the structure and function of synaptic transmission within the enteric nervous system essentially began in the early 1970's, and mushroomed through the 1980's to provide extensive and detailed informa­ tion that Furness & Costa brought together in 1987 in their elegant and comprehensive treatise (37). More recently, Mihara (76) has provided a major update on the chemical coding and electrophysiological properties of enteric neurons. This chapter focuses on recent contributions to our under-

Visceral afferents: their contribution to ‘sympathetic dependent’ pain

Abstract: For 80 years the sympathetic nervous system has been implicated in certain human pains, notably causalgia and reflex sympathetic dystrophy. This assumption has led to the accepted concept of 'sympathetic dependent' pain. In this critical review, the evidence for this assumption is assessed. It is found that the clinical phenomena suggesting sympathetic nerve involvement may be more satisfactorily attributed to effects of neuropeptides released from afferent C-fibres. The evidence also demonstrates that the effects resembling sympathetic dysfunction relate neither to the pain nor to pain relief following sympathetic blockade. The techniques and results of sympathetic blockade have rarely been adequately evaluated, and the apparent efficacy, specificity and mode of action of peripheral sympatholytic drugs are questioned. An alternative explanation is proposed: that visceral afferents subserve a number of human pains, including those that have been considered sympathetically mediated. Problems of terminology are discussed; use of the term 'visceral afferent' is clarified and broadened to include afferents, particularly those related to blood vessels, which travel within autonomic nerves, in addition to the classical visceral afferent innervation of the organs of the great body cavities. The clinico-anatomical evidence reviewed here indicates that this general and widespread system of afferents could subserve certain pains. The relationship between visceral afferents, somatic afferents and autonomic efferents is outlined, and support is found for the unitary nature of the sensory system envisaged by Langley. Conflicting results from experiments on animals and clinical studies in man on the pain-subserving properties of visceral afferents are summarized; these confirm that visceral afferents can, at least on occasions in man, mediate pain not considered typically 'visceral'. This conclusion receives support from a number of clinical observations: not only are diseases of the autonomic nervous system painless, but damage to previously painless autonomic nerves can generate pain, as illustrated by several different conditions; pain from diseases other than of the viscera of the great cavities and which involves the widespread visceral afferents may be alleviated by sympathetic blockade, presumably since afferents travelling within autonomic fibres are simultaneously blocked; and diseases which impair the function of autonomic nerves may be unexpectedly painless. The central nervous system sequelae following involvement of visceral afferents are outlined and found to be relevant to phenomena sometimes seen with causalgia and related conditions: spread of pain; mirror involvement; associated features such as involuntary movements; and referred pain. Visceral afferents are generally clinically silent unless damage occurs.(ABSTRACT TRUNCATED AT 400 WORDS)

Modulation of autonomic nervous system adjustments to heat stress by central ANG II receptor antagonism.

Abstract: The purpose of this study was to determine whether central angiotensin II (ANG II) participates in mediating selected sympathetic nervous system and neuroendocrine adjustments to heat stress in conscious freely moving rats. Mean arterial pressure (MAP), heart rate (HR), splanchnic sympathetic nerve activity (SpNA), plasma arginine vasopressin (AVP) concentration, and colonic temperature were measured before and during whole body heating (42 degrees C ambient temperature). Heating was stopped when a colonic temperature of 41 degrees C was attained. On consecutive days, rats received an intracerebroventricular (icv) injection of saline (0.9%) or 25 micrograms of the ANG II AT1-selective receptor antagonist losartan 20 min before the start of heating. Neither treatment influenced control levels of any parameter. The increase above baseline for MAP at the end of heating was attenuated by > 50% in the losartan, compared with the saline trial (P < 0.05), while HR remained unchanged from control values for both trials. Pretreatment with losartan icv eliminated the increase in SpNA observed during the heating period in the saline trial. Furthermore, the magnitude of change in plasma AVP during heating was significantly elevated in rats after icv administration of saline compared with losartan. These findings indicate that central ANG II receptor antagonism significantly attenuates the heating-induced elevations in MAP, sympathetic neural activity to visceral regions, and plasma AVP and suggest that the central nervous system actions of endogenous ANG II are required for full expression of the sympathoexcitatory, pressor, and neuroendocrine responses associated with nonexertional heat stress in the conscious rat.