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The autonomic nervous system (ANS) is an extensive neural network whose main role is to regulate the internal environment, by controlling homeostasis, hemodynamics and visceral functions.
The sympathetic activation, in addition to regulate the blood pressure, most likely also contributes to left ventricular hypertrophy, and to the commonly associated metabolic abnormalities of insulin resistance, obesity and hyperlipidemia.
In addition, the sympathetic activation affects involuntary body functions perspiration and digestion.
Finally, observing the marked vasomotor and sudomotor changes after traumatic nerve injury, it became apparent long ago that the ANS plays an important role in pain modulation and perception.
ANS diseases, sometime provoke autonomic neuropathy which refers to damage to the autonomic nerves. This damage disrupts signals between the brain and portions of the autonomic nervous system, such as the heart, blood vessels and sweat glands, resulting in decreased or abnormal performance of one or more involuntary body functions.
Autonomic neuropathy can be a complication of a number of diseases and conditions. And some medications can cause autonomic neuropathy as a side effect.
Therefore, the role of the autonomic nervous system is significant in several medical fields such as cardiologists, neurologists, gastro-enterologists, urologists, endocrinologists and chiropractors.
Because of its many functions, a complete assessment of the ANS is extremely complex.
Each specialty has developed its own test battery to assess those ANS functions most relevant to its field.
The ANS has components at every level of the nervous system. The central component, also known as the central autonomic network (CAN), includes the insula, medial prefrontal cortex, hypothalamus, amygdala, ventrolateral medulla, nucleus of the tractus solitarius (NTS), nucleus parabrachialis, periaqueductal gray, and the circum ventricular organs.
The hypothalamus is the most important ANS organ, controlling every vital function and integrating neuroendocrine, thermal and autonomic systems.
The peripheral components of the ANS are the sympathetic and parasympathetic nervous systems.
Parasympathetic preganglionic neurons lie in cranial and sacral nuclear groups. The parasympathetic nervous system acts selectively because the preganglionic axons synapse in ganglia that lie in close proximity to the effector organs.
The sympathetic system preganglionic neurons lie in the intermediolateral column of the spinal cord: their axons synapse in the prevertebral and para-vertebral ganglia from where postsynaptic fibers travel a relatively long distance to innervate each organ.
Unlike the parasympathetic system, the sympathetic is a diffuse system, able to generate responses from the adrenal medulla, post sympathetic adrenergic branch, post sympathetic dopaminergic branch and post sympathetic cholinergic branch.
The sympathetic and parasympathetic systems usually oppose each other, but in a few organs their effects are synergistic.
Neurotransmitters and ANS organization .
Acetylcholine (Ach) is the "classic" neurotransmitter for preganglionic neurons in the parasympathetic nervous system and it stimulated the M2 receptors and acts on different organs. The parasympathetic division functions with actions that do not require immediate reaction. It has an inhibitor action except in different functions summarize as SLUDD (salivation, lacrimation, urination, digestion, and defecation).
The Sympathetic system general action is to mobilize the body's nervous system fight-or-flight response. It is, however, constantly active at a basal level to maintain homeostasis. It has a stimulator action on internal organs except in SLUDD.
It is known to increase the heart rate and force of contraction, however, at the analysis of the receptors and neurotransmitters of the different branches, the actions are more complex.
Activation of adrenal medulla provides the release into the blood of epinephrine (E) and norepinephrine (NE) and it stimulated α and β receptors and acts in particular on heart and vessels.
Post sympathetic adrenergic stimulation release norepinephrine (NE), and it stimulated α and β receptors and acts on heart and vessels.
Post sympathetic cholinergic stimulation release acetylcholine, then nitric oxide and prostaglandins which provide vasodilation and sweat rate response. It stimulated the M2 receptors and acts on sweat glands and vessels.
Post sympathetic dopaminergic stimulation release dopamine and increased in renal blood flow and excretion of sodium (natriuretic action). It stimulated the D1 receptors and acts on renal vessels.
Current scientific knowledge:
Neurotransmitter effects on cardiovascular system
Effect of acetylcholine: reduce the heart rate and force of contraction of heart .
Effects of Epinephrine: Increased the Heart rate, cardiac output and systolic blood pressure.
Effects of Norepinephrine: Increased the Heart rate, cardiac output and systolic and diastolic blood pressure and provoke vessel vasoconstriction.
Effects of Nitric oxide: vasodilation via the vascular endothelial cell function. It is known as the endothelium-derived relaxing factor', or 'EDRF', and decreased of Nitric oxide is associated with cardiovascular risk and increased of reactive oxygen species (ROS). The NO released from the post sympathetic cholinergic branch affect the microcirculation (capillary).
Effects of prostaglandins: There are a variety of physiological effects; however, the prostaglandins released from the post sympathetic cholinergic branch affect the microcirculation (capillary) and can provoke inflammatory response and pains associated with the release of bradykinin.
Effects of Dopamine: vasodilation via the renal vessel and increased the renal excretion. The dopamine release is link to the nitric oxide release and counteracts the angiotensin-renin system.
At the lecture of the ANS neurotransmitters effects, it is evidence in pivotal position of ANS and in particular the different branches of sympathetic activation in blood pressure regulation with vasodilation/vasoconstriction balance.
Because postganglionic fibers are unmyelinated, they cannot be tested directly by conventional neurophysiologic techniques, i.e., nerve conduction studies and electromyography. Therefore, the only way to assess their function is indirect, by evaluating the response elicited reflex by appropriate stimuli.
Actual Methods of ANS diagnosis
Electrophysiological methods measuring ANS are
2. Neurochemical techniques providing quantification of noradrenaline spillover to plasma could be useful guide to sympathetic system function.
New approach in combination of technologies to asses ANS activity level in fast way and low cost:
ES Complex Software is software for use with the following models with management capabilities: a) blood pressure device, b) oximeter device, c) galvanic skin responses device and d) bioimpedance device. When use combination, the ES Complex software enhances the data management.
ES Complex medical data
The Blood pressure device provides systolic and diastolic pressure
The oximeter ( ESO device) provides arterial stiffness and HRV analysis and testing (Valsalva and orthostatic tests)
The galvanic skin response (EIS-GS device) provides the sweat rate response following constant electrical stimulation.
And the bioimpedance device provides estimation of the body composition.
Despite the proposed methods of ANS assessment, autonomic tests using neurophysiologic and neurochemical methods, until very recently, were available only in a few specialized centers. Now, the methods to measure noninvasively cardiorespiratory and circulatory parameters and to measure sweat production are commercially available. The cost of establishing a lab, however, is about $66,000, and reimbursement remains a major problem. The testing is time consuming, averaging 1 hour per patient. Furthermore, skilled technicians and physicians trained in correctly interpreting the studies are few. Adequate baseline acclimatization and proper positioning of subjects are crucial.
The neurochemical way to assess the ANS noradrenaline spillover to plasma has a major limitation: The deficiency is the dependence of plasma norepinephrine concentrations on rates of removal of the neurotransmitter from plasma, not just sympathetic tone and noradrenaline release. Plasma norepinephrine measurements can be misleading in heart failure research, because the rate of removal of norepinephrine from plasma is slowed due to reduced cardiac output and regional blood flows . Drugs such as angiotensin converting enzyme-inhibitors, having beneficial hemodynamic effects, will increase regional blood flows, increase norepinephrine plasma clearance and, as a consequence, lower the plasma concentration of the neurotransmitter in heart failure, which may be misinterpreted as a reduction in sympathetic nervous activity.
Heart rate in time domain and power spectral analysis techniques are commonly applied to estimate the parasympathetic level activity and as an alternative, noninvasive method for studying sympathetic function in the heart. With this technique, mathematical partitioning allows identification of individual, superimposed rhythms producing cyclical variation in heart rate and arterial pressure. The autonomic nervous system provides the principal effector mechanism for heart rate variability. Although the low-frequency heart rate variability (approximately 0.1 Hz) derives in part from the influence of the cardiac sympathetic nerves, it does not provide a valid measure of all the branches of the sympathetic system.
The ES Complex software managing the data of recognized neurophysiologic methods (HRV analysis and testing , GSR and blood pressure measurements) could provided a new fast approach of ANS assessment at effective cost .