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Results for “Sympathetic Nervous System”

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PubMed1990

[The function of the sympathetic nervous system and its behavior during regional anesthesia].

The activity of the sympathetic nervous system is of fundamental importance in the regulation of vital bodily functions. Impairment of sympathetic neuronal efferences results in considerably disordered effector function, and in some cases even in complete failure. Clinically, this is of great significance, because if an anesthetic agent produces cause the sympathetic system to block, the effects can be serious in individual cases, particularly on the cardiovascular system. If complications are to be avoided, it is essential to assess the degree of block correctly. Clinical monitoring has a variety of applications, a particularly useful one being measurement of the sympathetic system during regional anesthesia, for which quantification of the blocking effect is a clinical necessity and the degree of block needs to be ascertained without delay, for example in the case of spinal or peridural anesthesia. The activity of the sympathetic system can be monitored indirectly by two means: by measuring changes in skin temperature (with reference to all circulatory parameters), as these reflect its influence on the arterioles, and by measuring the skin resistance caused by the eccrinal sweat glands, which are also regulated by the sympathetic system. As the anatomical and functional structure of the system is highly complex a connection between the two measurements cannot necessarily be assumed. The two variables were measured simultaneously during spinal anesthesia and analysed. It was shown that the two measurements correlated well, at least in the statistical middle range, and that skin resistance was by far the faster and more sensitive of the two.

Anesthesia, Conduction↗

PubMed1998

[Sympathetic nervous system and pain--some open questions].

BACKGROUND: Neuropathic pain syndromes may be treated by intervention at the sympathetic nervous system. The pain in these syndromes is therefore called sympathetically maintained pain (SMP). Typical disorders with a SMP component are complex regional pain syndromes (reflex sympathetic dystrophy and causalgia), traumatic neuralgias and herpes zoster. RESULTS: Open questions are how the efferent sympathetic nervous system is capable of influencing pain sensation and which mechanisms underly the autonomic dysregulation often observed in these syndromes.(1) Somatic afferents that project through the sympathetic trunk do not exist. Therefore, a pure sympathetic block does not block afferent information arising from the affected extremity. What alternatives are possible? Under pathophysiological conditions a functional interaction of efferent sympathetic fibers and afferent nociceptive fibers could be demonstrated in patients and animal studies. The intensity of this coupling varies considerably between individual patients and is not necessary for the diagnosis of the disorder. (2) Sympathetically maintained pain and signs of autonomic dysfunction are independent clinical and pathophysiological phenomena without any causal relation. However, it is possible to treat both the SMP and the autonomic dysfunction with sympathetic blocks.

English Abstract↗

PubMed2000

Sympathetic nervous system activation in essential hypertension, cardiac failure and psychosomatic heart disease.

Regional sympathetic activity can be studied in humans using electrophysiological methods measuring sympathetic nerve firing rates and neurochemical techniques providing quantification of noradrenaline spillover to plasma from sympathetic nerves in individual organs. Essential hypertension: Such measurements in patients with essential hypertension disclose activation of the sympathetic outflows to skeletal muscle blood vessels, the heart and kidneys, particularly in younger patients. This sympathetic activation, in addition to underpinning the blood pressure elevation, most likely also contributes to left ventricular hypertrophy, and to the commonly associated metabolic abnormalities of insulin resistance and hyperlipidaemia. Antihypertensive drugs, such as moxonidine, which act primarily by inhibiting the sympathetic nervous system, should have additional clinical benefits beyond those attributable to blood pressure reduction, in protecting against hypertensive complications. Obesity-related hypertension: Understanding the neural pathophysiology of hypertension in the obese has been difficult. In normotensive obesity, renal sympathetic tone is doubled, but cardiac noradrenaline spillover (a measure of sympathetic activity in the heart) is only 50% of normal. In obesity-related hypertension, there is a comparable elevation of renal noradrenaline spillover, but without suppression of cardiac sympathetics (cardiac sympathetic activity being more than double that of normotensive obese and 25% higher than in healthy volunteers). Increased renal sympathetic activity in obesity may be a 'necessary' cause for the development of hypertension (and predisposes to hypertension development), but apparently is not a 'sufficient' cause. The discriminating feature of the obese who develop hypertension is the absence of the adaptive suppression of cardiac sympathetic tone seen in the normotensive obese. Heart failure: In cardiac failure, the sympathetic nerves of the heart are preferentially stimulated. Noradrenaline release from the failing heart at rest in untreated patients is increased as much as 50-fold, similar to the level seen in the healthy heart during near-maximal exercise. Activation of the cardiac sympathetic outflow provides adrenergic support to the failing myocardium, but at a cost of arrhythmia development and progressive myocardial deterioration. Psychosomatic heart disease: No more than 50% of clinical coronary heart disease is explicable in terms of classical cardiac risk factors. There is gathering evidence that psychological abnormalities, particularly depressive illness, anxiety states, including panic disorder and mental stress, are involved here, 'triggering' clinical cardiovascular events, and possibly also contributing to atherosclerosis development. The mechanisms of increased cardiac risk attributable to mental stress and psychiatric illness are not entirely clear, but activation of the sympathetic nervous system seems to be of prime importance.

Heart Diseases↗

PubMed1998

[Sympathetic nervous system and pain: pathophysiological mechanisms].

Sympathetic postganglionic neurons may be involved in the generation of pain, hyperalgesia and neurogenic inflammation under pathophysiological conditions. Experiments on animal models show that two categories of influence of the sympathetic neuron on afferent neurons can be distinguished and this distinction seems to be related as to whether sympathetic-afferent coupling develops after nerve lesion or after tissue trauma with inflammation. (1) Peripheral nerve lesion generates plastic changes of the afferent and sympathetic postganglionic neurons. This may lead to chemical coupling between sympathetic and afferent neurons which may entail activation and/or sensitization of primary afferent neurons by the sympathetic neurons. The mediator is probably noradrenaline and the afferent neuron expresses or upregulates functional adrenoceptors. The coupling may occur at different sites of the primary afferent neuron, e. g., at the lesion site, remote from the lesion site in the dorsal root ganglion or between nonlesioned sympathetic and afferent neurons which show collateral sprouting. The biochemical signals which trigger these changes probably are neurotrophic substances and their receptors which are synthesized by the peripheral neurons, Schwann cells and other cells in response to the peripheral lesions. (2) Sympathetic nerve terminals in peripheral tissues may serve as mediator elements in hyperalgesia and during inflammation following tissue trauma without nerve lesion. This function is largely independent of activity in the sympathetic neurons and independent of vesicular release of transmitter substances. The signals are probably synthesized and released from the sympathetic terminal or in association with it and belong to the prostaglandins (probably PGE(2) or PGI(2)). Furthermore, nerve growth factor (NGF) has a hyperalgesic action in inflammation which is at least in part dependent on the sympathetic nervous system.

English Abstract↗

PubMed1984

Effects of dietary sodium on sympathetic nervous system control of cardiovascular function.

The body of information which characterizes the adaptations in sympathetic nervous system control of cardiovascular function that occur in response to changes in dietary sodium intake is rapidly expanding. Multiple sites within the nervous system have been shown to be sensitive to variations in sodium availability, including the baroreceptors, cardiovascular regulatory centres in the brain, and the peripheral sympathetic neurones. In addition, dietary sodium is known to influence the level of activity of hormonal systems which are capable of modulating sympathetic neuronal function. The hormonal system that has been most widely investigated with respect to interactions with sympathetic neurones is the renin-angiotensin system. Other hormonal systems such as the prostaglandins, kinins, and natriuretic hormone have also been linked to sodium homeostasis. However, much less is known about their role in modulating sympathetic activity in response to alterations in sodium intake. Further elucidation of the interactions between dietary sodium and sympathetic neural control of the cardiovascular system should add significantly to our understanding of the mechanisms involved in cardiovascular regulation.

Animals↗

PubMedDate not supplied

Elevated sympathetic nervous system activity in patients with recently diagnosed rheumatoid arthritis with active disease.

OBJECTIVE: To investigate sympathetic (SNS) and parasympathetic (PNS) nervous system activity in patients with recently diagnosed rheumatoid arthritis (RA), and to analyze the association between activity of these systems and disease activity, and complaints that frequently occur in RA, viz., pain, fatigue, negative mood, and stiffness. METHODS: To assess sympathetic and parasympathetic nervous activity, the Pre-Ejection-Period (PEP) and Respiratory Sinus arrhythmia (RSA) were measured on two consecutive nights in a real-life environment in 25 patients with RA [19 female (f), 6 male (m), mean age 55.2 years) and 28 healthy controls (20f, 8m, mean age 55.8 years]. RESULTS: Patients showed a significantly shorter PEP (reflecting elevated SNS activity) compared to healthy controls, an effect that was most pronounced in those with active disease. RSA and the heart period did not differ between patients and healthy controls. The heart period was significantly associated with stiffness, but neither PEP nor RSA were associated with pain, fatigue, mood, or stiffness. CONCLUSION: Our study showed that cardiac sympathetic nervous system activity is elevated in RA, whereas cardiac parasympathetic activity remains at a normal level. Our results suggest that inflammatory stress rather than the common symptoms of RA challenge the SNS.

Arrhythmia, Sinus↗

PubMed1986

Sympathetic nervous system trophism for neuroblastoma and its age dependence in rats.

The sympathetic nervous system modulates the growth of C-1300 mouse neuroblastoma in vivo and in vitro. We now report that a mitogenic/trophic factor that augments growth of C-1300 neuroblastoma and of the S-20 neuroblastoma clonal line is present in freshly excised sympathetic cervical ganglia from newborn rats, but is not detectable in homogenates from sympathetic ganglia obtained from adult rats.

Age Factors↗

PubMed1997

Role of sympathetic nervous system in cardiovascular effects of centrally administered endothelin-1 in rats.

Centrally administered endothelin-1 (ET-1) produces a biphasic response, an initial increase followed by a decrease in blood pressure (BP). The pressor effect is due to stimulation of the sympathetic nervous system and/or release of vasopressin. The mechanism responsible for the depressor effect after central administration of ET-1 is still not known. Systemic and regional circulatory effects of intracerebroventricular (i.c.v.) administration of ET-1 (100 ng) were determined in anesthetized rats, using a radioactive microsphere technique. BP, cardiac output, and stroke volume were significantly decreased 30, 60, and 120 min after central administration of ET-1. Heart rate and total peripheral resistance were not altered. ET-1 produced a reduction in blood flow to the brain (83%), heart (62%), kidneys (53%), gastrointestinal tract (43%), portal system (46%), and musculoskeletal system (55%). To determine the role of the central nervous system in cardiovascular effects of centrally administered ET-1, experiments were performed in cervical-sectioned rats. The changes in systemic and regional blood circulation induced by centrally administered ET-1 in normal rats were not observed in cervical-sectioned rats. Pretreatment with a specific antagonist of ETA receptors, BQ-123 (10 micrograms i.c.v.), antagonized systemic and regional circulatory effects of ET-1. Centrally administered clonidine (1 microgram i.c.v.) produced hypotension and bradycardia, known to be mediated through the sympathetic nervous system. Pretreatment with an ETA receptor antagonist, BMS-182874 (50 micrograms/kg iv), blocked clonidine-induced hypotension and bradycardia. We conclude that centrally administered ET-1 stimulates ETA receptors to produce systemic and regional circulatory changes mediated by the sympathetic nervous system.

Animals↗

PubMed2000

The activity of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system in relation to waist/hip circumference ratio in men.

OBJECTIVE: To investigate possible differences, between generally and abdominally obese men, in activity and regulation of the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system. RESEARCH METHODS AND PROCEDURES: Fifty non-diabetic, middle-aged men were selected to obtain two groups with similar body mass index (BMI) but different waist/hip circumference ratio (WHR). Measurements were performed of the activity of the HPA axis and the sympathetic nervous system, as well as metabolic and endocrine variables. RESULTS: Men with a high WHR, in comparisons with men with a low WHR, had higher insulin, glucose, and triglyceride values in the basal state and higher glucose and insulin after an oral glucose tolerance test. Men with high WHR had elevated diurnal adrenocorticotropic hormone (ACTH) values but similar cortisol values, except lower cortisol values in the morning. Diurnal growth hormone concentrations showed reduced peak size. Stimulation of the HPA axis with corticotropin-releasing hormone (CRH) and laboratory stress showed no difference in ACTH values between groups, but cortisol values were lower in men with high WHR. In comparison with men with a low WHR, men with a high WHR had elevated pulse pressure and heart rate in the basal state and after challenges by CRH and laboratory stress. They also had increased urinary excretion of catecholamine metabolites. DISCUSSION: These results suggest a mild dysregulation of the HPA axis, occurring with elevated WHR independent of the BMI. The results also indicate a central activation of the sympathetic nervous system, such as in the early phases of hypertension, correlating with insulin resistance.

Adipose Tissue↗

PubMed1950